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The HIV Puzzle

In response to the latest developments in HIV/AIDS dissidence the Perth Group has distributed the following document, full of the original in-depth analysis one has come to expect from them – and only them – among dissidents.

Claus Jensen

 

The HIV Puzzle

 

I. What is being measured?

We all agree there is a correlation between something measured in the blood and the probability a person has or will develop what presently are known as AIDS indicator diseases.  But what is being measured?  There are four disparate views which cannot all be correct.

  1. HIV protagonists assert what is being measured is antibodies specific to antigens unique to a retrovirus HIV, or similarly the unique nucleic acid sequences (plasma RNA “viral load” or HIV DNA “viral burden”).
  2. Peter Duesberg agrees with the protagonists, differing that “A virus is a potential pathogen, [but] an antibody is a certain antidote” and hence the retrovirus is harmless.  It is not clear whether the virus is present and harmless (neutralised by the “antidote”) or absent and harmless (eliminated by the “antidote” and hence, contrary to the theory of retroviruses, its DNA does not reside within the cellular genome).  It would help if Duesberg clarified his meaning.

The protagonist and Duesberg views are based on proof for the existence of a unique retrovirus.  This seminal topic has been argued in published papers and other places by the Perth Group many times dating back to 1988 and most recently in Brent Leung’s documentary The Emperors New Virus? and our accompanying commentary.  www.theperthgroup.com/OTHER/envcommentary.pdf

  1. The Perth Group argues the test kit antigens and nucleic acid sequences are non-retroviral, that is, they are cellular.
  2. Etienne de Harven asserts the “viral load” measures the DNA of endogenous retroviruses but has not provided an explanation of the origin of the antibody test kit antigens.  Thus it would be speculative to comment on his views on the antibodies that react with these antigens.

Over the past few years we have repeatedly argued with de Harven and Andrew Maniotis about “human endogenous retroviruses” (HERVs), “endogenous retroviral sequences” and “viral load” measurements.  Since it appears even people who should know better such as David Crowe still think we “aren’t totally clear on this matter” let us repeat our views.

de Harven has declared all the dissidents who precede him wrong.  By the mid-2000s he was claiming to be the first person to clarify why Montagnier had proof for the existence of a “TYPICAL [endogenous] RETROVIRUS” but no proof for the isolation of “HIV” and thus for its existence.  More importantly it was he (de Harven) who worked out the correct answer to “The HIV Puzzle – what is being measured?”.   As US senator the late Daniel Moynihan put it, “everyone is entitled to his own opinion, but not to his own facts”.   Here we argue de Harven has made several errors of fact and thereby considerably muddied the waters.  We also give a summary of our answer to the above question.

Initially de Harven claimed the “HIV” viral load measures DNA of endogenous retroviruses originating in the “nuclei” of “peripheral blood mononuclear cells”.  This is wrong.  “Viral load” is a measurement of “HIV” RNA present in plasma.  In other words de Harven did not appreciate which nucleic acid is measured or whence it originated.  If de Harven’s claim is to be believed, since “endogenous  retroviruses” are present “in all of us”, “all of us” should have a positive viral load test and its “measurement” should be the same in all of us.  Since AIDS patients have the lowest circulating T4 lymphocytes counts their “viral load” should be lower than seronegative individuals who typically have higher T4 cell counts.  This is not the case and alone is more than sufficient to argue there is no scientific basis for de Harven’s claim of being the only dissident to give a “satisfactory explanation” of “HIV”.

When de Harven’s attention was drawn to the above facts he quietly redefined the “HIV” viral load test without specifying who or what led him to change his mind.  In JAPS 2010 he wrote:  “Since 1996, real-time PCR has been used to claim quantification of a postulated HIV viremia, termed “viral load,” in AIDS cases.  These methods have been based on the study of patients’ plasma samples:  initially, samples originated from nuclei of peripheral blood mononuclear cells, and later from low-speed centrifugation pellets of plasma83”.  In reference 83 three methods for measuring “HIV” viral load are described.  None involve DNA originating from peripheral blood mononuclear cells or from plasma.  To the contrary, the author repeatedly refers to the “measurement” as “HIV-1 RNA” and “plasma HIV-1 RNA levels”.  Indeed  (a)  if as de Harven claims viral load measures “postulated HIV viremia”; (b) by definition viremia means virus particles in the blood; (c) retroviral particles contain RNA not DNA, it is patent nonsense to claim the HIV viral load measures DNA whatever its origin.  For some unknown reason de Harven does not know or does not want to know that by definition viral load measures the number of “HIV” RNA copies in plasma.  Instead he expounds to anyone willing to listen that viral load measures “the number of HIV particles hypothetically present in the circulating blood” and is a method for the “isolation of retroviral particles”.

Incredibly de Harven still claims “quantifying a presumed “viral load” has, therefore, probably nothing to do with an exogenous “HIV”.  It simply reflects variable amounts of circulating DNA”.  However, in an effort to correct his initial version of “viral load” he currently asserts the DNA does not originate in peripheral blood mononuclear cells but “from low-speed centrifugation pellets of plasma”.  In other words the only difference between his first “satisfactory explanation” of “HIV” and new one is that the DNA originated from low speed centrifugation pellets and not from the nuclei of peripheral mononuclear cells.

As an absolute minimum his claim that “HIV” viral load “measures” endogenous retroviruses requires proof for the existence of endogenous retroviruses.  Neither he nor anybody else has presented proof for the existence of endogenous retroviruses.  In fact the authors of the papers he claimed prove the existence of such retroviruses contradict him.  All retrovirologists, including the “HIV” experts agree no such proof exists.  According to Fauci and Gallo “there are no known human endogenous retroviruses”, a fact Gallo reiterated when testifying during an Australian court case in 2006/2007.  de Harven tried his best to convince us that endogenous retroviruses do exist.  However after being faced with the above evidence he still claims “The existence of human endogenous retroviruses has been known for some time” but adds:  “HERVs [human endogenous retroviruses] are fundamentally endogenous, non-infectious, vertically transmitted, defective viruses”.  A virus is a virus.  The main properties of viruses are their being particles and being infectious, that is, they are transmittable from cell to cell or, in what amounts to the same thing, from person to person.  If the particles are defective or non-transmittable they are not, were not and can never be viruses.

If a patient becomes infected with a given retrovirus, whether it originated on Venus or in himself it makes no difference to its subsequent behaviour, that is, its infectivity and pathogenicity.  For a particle originating in A to be a virus it must be transmissible to B and then from B to C and so on.  In A it may be endogenous but in B and C is exogenous.  If it arises de novo in all of A, B, C, then it is not a virus.

If endogenous retroviruses were to exist then to claim that the “HIV” viral load “measures” endogenous retroviruses and not “HIV” one must have proof  that the ultimate origin of the PCR primers used for “HIV” “measurements”  are derived from purified endogenous retrovirus particles.  This is a fact on which all virologists and retrovirologists, including “HIV” experts agree (see The Emperor’s New Virus?).  Neither de Harven nor anybody else has presented such proof and since there is no proof for the existence of endogenous retroviruses such proof is unobtainable.

Lately de Harven has diverted his attention from endogenous retroviruses to endogenous retroviral sequences.  Again, to claim that the “HIV” viral load “measures” “endogenous retroviral sequences”, the minimum absolutely necessary but not sufficient conditions are, in human (or animal) genomes:  there are DNA sequences whose expression, under appropriate conditions, leads to the synthesis of infectious retroviral particles (otherwise one has a misnomer).  Since no evidence exists for the presence in the human genome of DNA sequences which when expressed lead to the synthesis of retroviruses, some define the endogenous retroviral sequences as DNA sequences “made up of ancient relics of viral infections that occurred in our ancestors, which have been passed from generation to generation but are unable to produce infection”.  However there is no evidence for “ancient” retroviral infections.  They are called endogenous retroviral sequences because they were found to hybridise with the complementary DNA (cDNA) of exogenous retroviruses.  Obviously the relevant RNA will have to originate from purified retrovirus particles.  The question is, which retrovirus?  One of the best known retroviruses is the Friend Leukaemia Virus, which de Harven claims to have purified and thus proved its existence.  In fact de Harven and Friend never had such proof: http://www.tig.org.za/Friend.pdf.  The first, best known, most studied retrovirus, the virus in which the first “oncogene” was discovered and which subsequently led to the virus theory of cancer is the Rous sarcoma virus (RSV).  RSV is the gold standard for all other retroviruses including HIV.  Everybody credits Peyton Rous for its discovery in 1911 when he induced sarcoma in chickens by injecting them with cell-free filtrates (“filterable agent”) obtained from chicken sarcomas.  Remarkably “though the Nobel committee recognised the “agent” as a virus when it awarded Rous the [1966] Nobel prize for Medicine, he still refused to recognise it as such”.

Assuming endogenous retroviral sequences do exist, since by definition they are DNA sequences which hybridise with the cDNA of exogenous retroviruses, to claim “HIV” viral load “measures” “endogenous retroviral sequences” proof must exist that the PCR primers are the cDNA of purified exogenous retrovirus particle RNA.  No such proof exists.

Attempting to solve the “The HIV Puzzle – What is being measured?” entails two parts.  First, what chemical species is being measured?  Second, what is the genesis of that species?  Obviously one cannot answer the second without an understanding of the first.  de Harven still does not know what species is measured in the “viral load” test.  We all have the right to put forward any claim but, thanks to his perceived scientific status, perseverance and persuasiveness, all de Harven has managed to do is confuse many people including himself.

Before de Harven became a dissident the scientific and non-scientific literature contained evidence (of which he was fully aware) that:

(a)                questioned the role of “HIV” in AIDS pathogenesis;

(b)               postulated non-”HIV” theories of AIDS pathogenesis;

(c)                questioned the evidence which claimed proof for “HIV” isolation and purification and thus its existence;

(d)               gave a non-viral explanation for the “HIV” “measurements”, that is, both antibody and PCR tests.  (Endogenous retroviruses and endogenous retroviral sequences measurements were considered and discussed but on the basis of the scientific evidence were excluded).

The evidence for (c) was so significant that Montagnier, who recently told Brent Leung en camera purification is necessary “to prove you have a real virus” (see The Emperor’s New Virus?), when in 1997 was interviewed by the French journalist Djamel Tahi and questioned about the Perth Group’s claim admitted they did not purify any virus.  And furthermore the material they called “purified virus” did not contain retrovirus-like particles.  Charles Dauguet, the Pasteur Institute electron microscopist, also confirmed that all they ever had in their “purified” virus was cellular debris.  This being the case one has no choice but to conclude:

(a)                the antigens used in the “HIV” antibody tests are cellular proteins and the antibodies detected by the antibody test are either auto-antibodies or other “non-HIV” antibodies, that is, antibodies induced by “non-HIV” stimuli – “cross-reacting” antibodies.

(b)               the primers and probes used in “HIV” PCR are cellular nucleic acids, that is, the RNA “measured” by the viral load test has nothing to do with a retrovirus, “endogenous” or exogenous.

The facts that:

(i)                       the ultimate role of the viral DNA is to synthesise the viral proteins;

(ii)                     ample evidence (see The Emperor’s New Virus?) shows the “HIV” proteins are cellular proteins;

confirm yet again that “HIV” viral load is entirely divorced from retrovirus nucleic acids be they exogenous or “endogenous”.

The question then is, why does everyone not have a positive viral load “measurement”?

Let us recall that more than 60 years ago Nobel laureate Barbara McClintock showed that the cellular genome (DNA) can be restructured.  In her 1983 Nobel lecture she stated:  the “shock” which can lead to genomic reconstruction may be “either produced by accidents occurring within the cell itself, or imposed from without such as virus infections, species crosses, poisons of various sorts, or even altered surroundings such as those imposed by tissue culture…Many such mishaps and their adjustments would not be detected unless some event or observation directed attention to them” (emphasis added).

The RNA, which the “HIV” viral load actually “measures”, is even more fluid than the DNA.  The many post-transcriptional modifications include RNA editing.  “Sometimes editing is so extensive that the majority of sequences in a mRNA are not genomically encoded but are generated post-transcriptionally, producing the ‘paradoxical situation of a transcript that lacks sufficient complementarity to hybridise to its own gene!’.”  In other words the “viral load” RNA may not have a corresponding DNA.  No wonder then that everyone, including the CDC and the test manufacturers, state that “viral load” cannot be used to prove infection.  Little wonder no two “HIV” are the same.

Since the cultures from which the PCR primers originated and AIDS patients and those at risk have all been exposed to oxidising agents, which we have shown link all the AIDS risk groups, one will expect a positive “HIV PCR” “measurement” in these patients (and those exposed to similar agents) but not in healthy individuals.  There is ample evidence this is the case.

II.      LEGAL STRATEGIES

It goes without saying that, depending on the aim, legal strategies may vary according to particular circumstances.  Any win is welcome and dissidents who contribute to such outcomes are to be congratulated.  However cases can be won again and again forever without any consequences for the HIV theory of AIDS and thus for the millions of “HIV” positive people.  The question is what strategy can be used which will benefit not only one or a few individuals but all “HIV” positive people once and for all. Can we learn from previous cases?

 

Andre Parenzee

In 2006/2007 Andre Parenzee sought leave to appeal his recent conviction for endangering the lives of female sexual partners and transmitting HIV to one of them.  The Perth Group appeared as defence witnesses giving evidence there is no proof (a) for the isolation and purification of HIV and thus for its existence;  (b) HIV is sexually transmitted;  (c) antibody tests are specific for HIV.  With the benefit of hindsight arguing on three fronts was a serious mistake.  We should have confined ourselves to (a) but at the time decided to include (b) and (c) because we thought they would serve as a complementary buffer.  As everyone knows, from the beginning we questioned Luc Montagnier’s and Robert Gallo’s claims that they isolated and purified a new retrovirus (and thus proved its existence) from AIDS patients.  In fact arguing mostly on the data in Montagnier’s May 1983 Science paper the hearing progressed extremely well, as acknowledged by David Crowe.  So much so that after starting with two witnesses the prosecution ultimately called another six, including Gallo and Sir Gustav Nossal, an immunologist considered the doyen of Australian medical research.

After eight days giving evidence and then being cross-examined by the prosecution lawyers Crowe, and through him his associates, began to interfere behind our backs. It appeared they were as much interested in the survival of “HIV” as were the “HIV” experts.  Between them they convinced the defence lawyer to call Duesberg as an expert witness and to alter the appeal strategy from “there is no proof for the existence of HIV” to “there is no evidence that HIV causes AIDS”.  We objected on the basis that this “new” strategy would present the court with the impossible and dangerous spectacle of defence experts arguing between themselves.  (As it was, one of the prosecution experts testified that Duesberg accepts the existence of HIV).  The judge was made aware of this.  Having decided to change course midway through the hearing, the defence lawyer eventually informed the court that if the judge were to grant a retrial he would engage other experts and would most probably exclude the Perth Group.  In other words and as the Australian press recognised, the defence lawyer made his own witnesses non-experts and asked the judge to grant leave for a retrial on the basis of evidence nobody had yet presented to him.  Under these circumstances the judge had no choice but to find for the prosecution.  What is significant is that although the prosecution considered the isolation issue warranted engaging the likes of Gallo as well as several leading Australian experts, the defence lawyer failed to press his advantage during cross-examinations.  The Parenzee appeal, which started out with great promise, became an absolute disaster for the dissident movement.  Yet it did confirm that the Achilles heel of the HIV theory is HIV.

 

Sergeant TD

Recently there was a court case in the United States in which an HIV positive army sergeant was acquitted of “four HIV-related” criminal charges.  This result has been hailed a milestone, a dissident success.   Because we have not been able to obtain the court transcripts we are not in a position to make specific comments.  However we can make some general comments based on Rodney Richard’s affidavit and David Steele’s interview with Celia Farber.  http://www.omsj.org/2012/PRN-SgtTD.mp3

Richards accepts there are humans who have acquired HIV infection from other humans and lists five factors that must be satisfied in order to diagnose a person infected.  He states “the only valid determination on whether a patient is infected with HIV would be:  (1) a positive result from ELISA;  (2) a positive result from WB;  (3) a positive culture of the virus;  (4) risk factors consistent with the possibility of infection;  and (5) clinical symptoms characteristic of AIDS that cannot be accounted for by other factors”.

From Richards’s affidavit it appears there were three factors underpinning the defence case (all of which accept the existence of HIV and HIV antibodies and do not question HIV being the cause of AIDS):

1. HIV infection induces antibodies which neutralise and thus get rid of the virus.  As Richards affirms in his affidavit, “In fact, these antibodies assist in the elimination of the germ by binding to it, thereby interfering with its ability to replicate, and marking it for digestion by other cells in the immune system.  Furthermore, germ specific antibodies produced in this way remain at detectable levels in the body for several months to several years, even after the complete elimination of the infectious agent from the body”.

2.  Since antibodies cross-react the specificity of any HIV antibody test cannot be 100%.

3.  Biotechnology companies are at great pains to point out (via their packet inserts) that a positive test per se (antibody and PCR) is not proof of infection.

Any or all of these may have been sufficient to sway the judge in favour of Sgt TD, but in the absence of court documents any further comments would be speculative.

In our view, any leading HIV expert who might have testified at Sgt TD’s or a future trial could have countered the above points as follows:

1.  As is the case with many viruses and contrary to what Duesberg repeatedly asserts, HIV antibodies are not neutralising.  Even more so in the case of retroviruses.  “HIV” is claimed to be a retrovirus, which means that within hours of exposure its genome is incorporated into host DNA where it stays for as long as the host shall live.  Any HIV expert will testify this is what stands in the way of the Holy Grail of curing AIDS.   In fact Duesberg, who Richards retained and from whom he learnt about “HIV tests”, asserts there is 100% correlation between HIV DNA PCR and a positive antibody test.   That is, a positive antibody test = HIV infection hence antibodies do not eliminate the virus.   Once infected, always infected, and “our immune system will [never] get rid of the virus”.  Duesberg is also on record as saying that there is 100% correlation between a positive antibody test and a “positive culture of the virus”.  Since there is 100% correlation between antibodies,  PCR and culture there is no need to do all the tests.  One for example, the antibody tests, which is the cheapest and easiest, will suffice.

2.  There are many reports, famously chronicled by Christine Johnson, where antibodies react with one or two “HIV” proteins in the HIV test kits.  However, these reports do not equate to positive antibody tests because antibody testing is a sequence of tests and requires several particular antibodies for a positive result.  Even if they were to fulfil the criteria for a positive test they will do nothing more than support the notion of cross-reacting antibodies.  No antibody test is 100% specific and no HIV expert will argue the contrary.

3.  This point is related to 2.  Because antibodies induced by agent X can react with agent Y (cross-react) test results must be interpreted in light of clinical data.  This is a mathematical fact taught to every medical student.  One can get an intuitive feel for this as “the clinical data steering the test result in the right direction (and away from the wrong direction) for a particular patient”.  For example, during pregnancy the protein beta-HCG is secreted into the bloodstream by the placenta and its detection is used to diagnose pregnancy.  But if the clinical data are the patient is a 70 year old woman, or a man, then the cause is not pregnancy.  (The same protein may be detected in cases of testicular and other cancers).  Yes it’s true Sgt TD was well, not in a risk group and may have passed a blood donation screening questionnaire with flying colours.  However, there are two sides to Richard’s 5th point.  Certainly the defence can use it to argue its case but the prosecution could counterclaim that:  (a) while most infectious agents cause clinical manifestations within days to a few weeks of infection (short incubation period), this is not the case with HIV;  (b) the fact that an HIV positive individual is healthy does not preclude genuine, non-cross-reacting HIV antibodies being the cause of his positive test, that is, the test being a true positive (which Richards agrees does occur).  To the contrary:  an HIV expert would argue that a person who is healthy has no reason for having cross-reacting antibodies and hence a false positive test is virtually impossible.  Even more so if that person’s sexual partner is also HIV positive.  In regard to PCR it is true that Roche and the CDC advise that “viral load” is not to be used to diagnose HIV infection.  However, this is not the case for DNA PCR.  In fact Kary Mullis was a co-author of the first paper (1987) in which PCR was used to diagnose HIV infection.  And, as already said, we have Duesberg’s 100% correlation.

We are pleased events turned out well for Sgt TD, but how will a defence lawyer argue on the basis of points 1-3 where the accused is a gay man with a low T4 cell count who may also have had an AIDS defining condition and an HIV positive sexual partner?  Even in Sgt TD’s case a well informed prosecution expert witness could easily have argued that the two sequence antibody test (ELISA/WB, the normal practice in the US and Australia), has a  combined specificity so high it negates any possibility Sgt TD’s result is a false positive regardless of his excellent clinical state.  (Download the EXCEL file Overall sensitivity and specificity from combining screening tests; predictive value from http://www.epidemiolog.net/studymat/ ).  No doubt future trials will see a much better prepared prosecution calling experts highly familiar with antibody testing in general and “HIV” testing in particular.  Because of this, in our view it is highly doubtful Sgt. TD’s outcome will be repeated.

As far as we can tell the defence avoided the issue of HIV isolation and purification.  In other words, the existence of HIV was not challenged, which is in line with the desire of those dissident colleagues who believe this topic should be avoided at all costs.  Notwithstanding, anyone familiar with antibody testing will realise that in his affidavit Richards, perhaps unintentionally, does raise this particular issue:  “The reason that manufacturers of these more specific tests [WB] can offer no estimate of how probable it is that such a sample has antibodies to HIV, is because there is currently no recognised standard for establishing the presence or absence of [HIV] antibody in human blood”?  Richards further asserts that “standard” means “gold standard”.  If, as Richards and biotechnology companies accept there is no gold standard for the HIV tests, this means there is no mechanism to distinguish between true and false positive tests.  Yet as we have shown again and again beginning with our 1993 Bio/Technology paper there is a gold standard for the HIV antibody tests.  As in all tests it is the entity being measured.  This being the case asserting there is no gold standard for HIV antibody tests is asserting there is no HIV.  And if there is no HIV there can be no tests for HIV no matter what is measured.  How can there be an HIV test without HIV?  This is a main question which in future cases biotechnology companies and prosecution experts will have to answer.

ELENI, VAL & JOHN

July 31st 2012

The Perth Group

www.theperthgroup.com

ACKNOWLEDGEMENTS

We thank Anthony Brink, Claus Jensen and Rodney Knoll for their valuable assistance in the preparation of this document.

 

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Wesolowski et al: Fraudulent “HIV” Study Confirms Difference between True and False Positive is a Matter of Quantity not Infection with a Unique Retrovirus

He aquí la traducción al español de este artículo:

The observation originally made by the Perth Group that HIV has never been isolated, and that the existence of HIV therefore is in doubt predicts that the HIV tests are not specific to a unique viral entity. In The Circular Reasoning Scandal of HIV Testing, an article based on the Perth Group’s work, Neville Hodgkinson elaborates on the way it was determined which proteins belong to HIV in the absence of a proper isolate:

There is an association between testing HIV-positive and risk of developing Aids. This is the main reason why scientists believe HIV is the cause of Aids. But the link is artificial, a consequence of the way the test kits were made.

It never proved possible to validate the tests by culturing, purifying and analysing particles of the purported virus from patients who test positive, then demonstrating that these are not present in patients who test negative. This was despite heroic efforts to make the virus reveal itself in patients with Aids or at risk of Aids, in which their immune cells were stimulated for weeks in laboratory cultures using a variety of agents.

After the cells had been activated in this way, HIV pioneers found some 30 proteins in filtered material that gathered at a density characteristic of retroviruses. They attributed some of these to various parts of the virus. But they never demonstrated that these so-called “HIV antigens” belonged to a new retrovirus.

So, out of the 30 proteins, how did they select the ones to be defined as being from HIV? The answer is shocking, and goes to the root of what is probably the biggest scandal in medical history. They selected those that were most reactive with antibodies in blood samples from Aids patients and those at risk of Aids.

This means that “HIV” antigens are defined as such not on the basis of being shown to belong to HIV, but on the basis that they react with antibodies in Aids patients. Aids patients are then diagnosed as being infected with HIV on the basis that they have antibodies which react with those same antigens. The reasoning is circular.

Gay men leading “fast-track” sex lives, drug addicts, blood product recipients and others whose immune systems are exposed to multiple challenges and who are at risk of Aids are much more likely to have raised levels of the antibodies looked for by the tests than healthy people – because the antigens in the tests were chosen on the basis that they react with antibodies in Aids patients. But this association does not prove the presence of a lethal new virus.

If there is no unique HIV we can expect that the particular risk groups on the basis of which the “HIV” proteins were selected will continue to test positive more often than other groups, but we can also expect that they will test “almost positive” (“indeterminate” or “false positive”) more often than non-risk groups. Especially in the case of the screening tests, people from the risk groups will tend to have elevated levels of the relevant antibodies and therefore be closer to or above the cut-off level for a positive screening test result. Similarly, they will be more likely to test positive on at least some of the  proteins in the Western Blot test, and when they test positive on a predetermined number or  combination of proteins, the test is considered a true positive.

The non-isolation theory of HIV predicts that the difference between a false positive test and a true positive test result, everything else being equal, is a function of quantity (the number and severity of exposure to various antigens, such as semen and recreational drugs) rather than quality (exposure to a unique antigen, HIV), and that people from the original risk groups, gays, drug users etc. will test “almost positive” at higher rates than others because of their more frequent exposure to various antigens or health challenges in general.

As one would expect, the otherwise prolific HIV professionals have not been tripping over themselves to produce studies confirming the hypothesis that in any population the rate of false positive HIV tests will correlate with the rate of true positive tests, but  in their 2011 paper  False-Positive Human Immunodeficiency Virus Enzyme Immunoassay Results in Pregnant Women Wesolowski et al attempt to capitalise on the fact to promote their universal testing agenda. The paper is written to dispel what the authors consider the myth that pregnant women in low risk populations test false positive in unacceptably high numbers and therefore should not be tested.

The usual way to find out if something is worth the risk or the cost involved is to perform some form of cost/benefit analysis. In this case part of such an analysis would consist in finding out the ratio of false positives”to “true positives” one can expect to get ( (a true positive being defined as one in which the screening test and confirmatory test are both reactive).   To take an extreme example, if for every false positive screening test there were 10,000 “true positive” tests, universal testing would seem to be worth it. If on the other hand the ratio were 1 “true positive” test to 10.000 false positive tests, universal testing would be a lot less attractive.

Wesolowski et al. do  not tell us what ratio of false positives to “true positives” they find acceptable. This is likely because the result was not very impressive. As a matter of mathematical necessity the lower the prevalence of HIV positives in a population the higher the ratio of false positive tests to “true positive” tests will be; that is one of the main arguments for not targeting low prevalence populations for screening. In this case Wesolowski et al examined an extremely low prevalence population of pregnant women and predictably found that there were more than two false positive tests to every “true positive” test, corresponding to a positive predictive value (PPV) of only 30%. Wesolowski et al duly report these results, but in the discussion and conclusion little weight is placed on them and instead the rate, as opposed to the ratio, of false positives is emphasised:

 

False-positive HIV EIA results were rare and occurred less frequently among pregnant women than others. (…) False-positive antibody EIA test results are rare, so universal HIV screening among pregnant women should be pursued without hesitation unless a woman declines. However, clinicians should be aware that when HIV prevalence is low, as is often the case among pregnant women in the United States, a reactive EIA result is more likely to be false-positive.

Wesolovski et al. do not tell us what an unacceptable rate of false positives would be, just as they don’t tell us what an unacceptable ratio of false positives to “true positives” would be, but it is apparent that they are suggesting a yardstick. They picked a group of “others” (non-pregnant testers), which they compare with the pregnant group  in order  to be able to conclude that the rate of false positives among pregnant women is suitably low. We can thus infer that they consider the rate of false positives in the “other”, non-pregnant group to be very acceptable.

But there was an interesting difference between the pregnant and non-pregnant groups: The “true positive” prevalence in the non-pregnant group was more than 20 times higher than in the pregnant group (1.34% vs. 0.06%). That is hardly comparing like with like and Wesolowski et al can only get away with it because they focus exclusively on the rate not the ratio. The positive predictive value  (PPV) was in fact much higher in the non-pregnant group at 87% , which looks far more impressive in a cost/benefit analysis than the 30% PPV for the pregnant group.

Leaving that aside for a moment, let us take a look at Wesolowski’s breakdown of the numbers. There were 921,438 people in the pregnant group and 1,103, 961 people in the non-pregnant group, so the non-pregnant  group is larger by around a fifth, but the false positive and indeterminate rates in the non-pregnant group are much larger than this difference can account for.

Pregnant group – Non-pregnant  group

False positive (negative WB):                              951                 –              1,675

Indeterminate (indeterminate WB):                 306                 -                633

“True positive”  (positive WB):                             541                 –              14,788

The HIV testing industry has had more than 25 years to make the screening tests (EIA, ELISA) and the confirmatory test (WB) correspond perfectly and still we see these large differences. For every two false positives in the pregnant, or low prevalence, group there were three in the non-pregnant, or high prevalence, group (o.14 vs. 0.21). And when it comes to indeterminate results the ratio is even higher at two to one.

Since pregnancy in itself is considered a risk factor for testing false positive, how come the false positive and indeterminate rates were so low in that group compared to the non-pregnant group? We propose the answer that the primary predictor of false positive rates in a given population is the “true positive” rate. Because of the lack of suitable studies it remains to be seen if this is always the case. If it is, this is strong evidence that the causes of a false positive  and a true positive test result are the same. In other words, the difference is quantitative rather than qualitative, just as the Perth Group’s and Neville Hodgkinson’s articles on the selection of the “HIV” proteins would suggest.

The objection could be made that in high prevalence populations the same behaviour that puts people at higher risk for HIV infection also puts them at higher risk for a number of other infections and conditions that can cause a false positive test result. In this way our hypothesis would be correct, the cause(s) of a false positive and a “true positive” test are the same, namely the same behaviour, but there would still be a qualitative difference, namely infection with a unique viral agent HIV. However, this presents a new problem: If it is accepted among HIV experts that people in the risk groups for HIV/AIDS are also at much higher risk for testing false positive what would be the point of Wesolovski’s study? Why compare a low prevalence population to a high prevalence population to see which has the highest false positive rates if it is already accepted that the primary predictor of the false positive rate is the “true positive” rate? Did Wesolovski et al publish a scientifically pointless propaganda piece for universal testing, whose outcome was assured in advance?

Special thanks to Colin Esperson, (AKA “Snout”, AKA Kevin Kuritzky) who made us aware of the Wesolowski paper and the sleight of hand involved in switching the focus from ratio to rate of false positives in low risk groups and consequently confirmed our suspicion that the paper was fraudulent propaganda. The productive discussion between MacDonald from the TIG team and Colin Esperson can be read in full here.

Claus Jensen

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Nonsense, Insults and Slander: Prof. de Harven Denies Charges of Plagiarism

De Harven did everything possible to indoctrinate people that he has done a great work in the past and now both Duesberg and the PG are wrong and only he is the greatest scientist.  The problem is that in the past the only thing he did was to contribute to messing up cancer research and now he is not even capable of doing a good job as a plagiarist. (The Perth Group, Jan 2012)

Ecco l’articolo tradotto in italiano

In an ongoing email exchange between the two, Steve Stannard directed Prof. de Harven’s attention to our last post and asked him to comment. We feel de Harven’s quite extraordinary answer deserves to be given in full for two reasons. The first is that we wish to give him every possibility to defend himself and show why we are wrong in our assessment of his paper and the second is that his answer illustrates so perfectly the mindset of the Rethinking AIDS orthodoxy.

Good evening Steve Stannard,

I apologize for late answering to your important Dec 29 note!  Sorry!

I must say that I was disturbed by several points in your note, and that’s probably why I hesitated to answer right away!

- I don’t know where Val Turner is finding his quotations, but I can tell you that I NEVER “admitted I never isolated any virus” !!!  To the opposite, for the past almost 50 years (!) I am proud for having achieved an excellent purification of these particles that were present in the blood of Swiss mice suffering from the Friend leukemia. True, at that time, we (Charlotte Friend, Peyton Rous, and me!) were convinced that these viruses were exogenous!  But could you ask Val Turner why he congratulated me in the late 90′s when I reproduced that famous picture in “Continuum”, and why he now seem to feel that this was rubbish!!!   Strange, don’t you think? (I attach that famous picture for your file!!)

- I was well aware about the fact that the PG had reviewed some data concerning endogenous viruses in the 90′s. But this was not their own work, from their own lab!!  They had reviewed OTHER PEOPLE’s WORK, and I don’t see why I should have included their reviews?  When I speak in my JAPS paper about HERVs and about circulating DNA, I carefully quoted Lower (77) and Anker (85) who are real molecular virologist/biologists, WORKING AT THE LAB BENCH!

- The old reviews by the PG (“Speculations on HIV DNA”) do not apply to my JAPS paper at all, because the indisputably NEW IDEA in my paper is for having associated HERVs and circulating DNA, something the PG never alluded to. If you can find any reference in which that critical association is being made before, please let me know!!

- You say that a note Val Turner wrote to me and Andy M. in July 2008 is a clear indication for the fact that Val T. is not ignoring my 2010 paper!!!

Strange, indeed!

- And to give a more recent perspective you sent me that piece by Claus Jensen that has apparently been presented at “The HIV Symposium”!!!

Could you tell me who sponsored that “Symposium”, please ?  Was this a scientific conference? Can hardly believe it!!   It is not enough to put Raphael’s ‘The School of Athens’ on top to make it scientifically valid!! I refuse to believe that Val Turner gives the slightest attention to Jensen’s piece that is an accumulation on non-sense and insults! When I first saw that piece I felt like suing Jensen for slander, but I have better things to do with my time! Val Turner should know that the fact that HIV research has been confounded by HERVs was first claimed, 2008, in Robin Weiss’s lab (C. Voisset’s paper, my ref. 92) and is not MY “major claim” as Jensen quite stupidly stressed!!!

- I verified with orthodox AIDS experts my difficulty to find any evidence for a key missing control, i.e. search for so-called “viral load” in SERONEGATIVE severely ill, non-AIDS patients (not babies, of course !). I corresponded with Jay Levy on that, and he could obviously not find such a reference either… (De Harven to Stannard, jan 2011)

If we take it from the top, the reader will note that de Harven only speaks of Val Turner, as if there were no other members of the Perth Group. We cannot tell if that is because the Perth Group uses Val Turner’s email address, or because he thinks Val Turner is the only Perth Group member worthy of mention, or simply because he has forgotten about the rest. The last explanation seems most likely since de Harven has also forgotten about his own published articles. For instance he informs us, “I don’t know where Val Turner is finding his quotations”. The quotation in question is from a letter by de Harven posted on the Rethinking AIDS website, where he writes:

These famous mouse leukemia retroviruses I have talked about so much (maybe too much!) have always been INTERPRETED as being exogenous, although their contagiousness has never been proved.

Not only has de Harven forgotten that he himself wrote, in support of his “new” theory of HIV, that he never proved the contagiousness (infectiousness) of his leukemia “retroviruses”, it seems that when he made that admission he had also forgotten his original papers where he claimed that the particles he purified were proven to be viruses precisely because they were infectious. This is a quote from the Perth Group’s analysis of de Harven’s early papers:

Since the injected filtrates transmitted “a disease having the character of a leukaemia” (because the filtrates were transmitting the disease especially a malignancy, it does not mean that the filtrates contained a virus, Rous pointed this out in 1911) and the particles were not seen in the nonleukaemic mice, in a paper published in 1960 de Harven and Friend arbitrarily decided to call the particle “virus” particles instead of “virus-like”. “The particles, however, will be referred to as “viruses” and no longer as “virus-like” since all specimens were checked for infectivity and proved capable of transmitting the disease”

The last sentence is a direct quote from de Harven and Charlotte Friend. Since de Harven now claims the particles were in fact not proved to be infectious although the filtrates were capable of transmitting disease where is the justification for calling them viruses instead of “virus-like”?

In terms of the HIV theory of AIDS, if we allow without proof that the non-infectious virus-like particles are endogenous retroviruses, and we also allow that they are capable of transmitting disease, how can we claim that “HIV” (larger than normal quantities of circulating endogenous retroviral DNA and particles, according to de Harven) is harmless?

In the last paragraph of his letter to Steve Stannard de Harven writes:

- I verified with orthodox AIDS experts my difficulty to find any evidence for a key missing control, i.e. search for so-called “viral load” in SERONEGATIVE severely ill, non-AIDS patients (not babies, of course !). I corresponded with Jay Levy on that, and he could obviously not find such a reference either…

De Harven is alluding to our and Duesberg’s observation that if “HIV” were an endogenous retrovirus, it would per definition be part of the human genome and the PCR tests should be able in principle to detect it in all of us. We wrote previously that we think de Harven has a good point about the lack of controls for the “HIV viral load”, but since de Harven defines “HIV” as any circulating endogenous retroviral DNA the question remains, why is it not detected more often for example in babies – even seropositive babies (babies of HIV positive mothers typically retain maternal antibodies for several months, which is why the PCR tests are considered more reliable for infants)? De Harven himself is in full agreement with the point that even “normal individuals” should be positive on the viral load tests:

Bingo: this is HIV!!!!!!   NO: it is the amplification of endogenous retroviral sequences that are present in ALL OF US! It has NOTHING to do with the hypothetical presence of circulating retroviral particles! It has nothing to do with any “measurement” of the “viral load”.  By that method, WE ALL have some level of …”viral load”!!!  Really? Yes, but to save the establishment from too much embarrassment NO CONTROL, on you and me, was ever made nor published!  Do you know the reference of one single paper in which a large group of “normal” individuals would have been studied for HIV “viral load” by PCR measurement? I don’t. (de Harven on RA site)

De Harven has now redefined “normal individuals (like) you and me” as “severely ill non-AIDS patients”, and further that babies “of course” do not qualify. A contradiction? Not exactly. Finding himself under pressure, de Harven has merely “borrowed” another point from the Perth Group, that the sequences defined as “HIV” often seem to arise as the result of pathological processes, or at least uncommon conditions, which is why they are in fact not present in all “normal individuals”.  If de Harven now admits that his “HIV” can only be found in severely ill people, he has also admitted that it is per definition not a human endogenous retrovirus, which is part of all of us all the time, although perhaps not at all times circulating at detectable levels in the bloodstream.

This brings us to de Harven’s defence against our plagiarism charges, which was the following:

Could you tell me who sponsored that “Symposium”, please?  Was this a scientific conference? Can hardly believe it!!   It is not enough to put Raphael’s ‘The School of Athens’ on top to make it scientifically valid!!

The readers will recognise the empty snobbery that has now become the standard reply by any Rethinking AIDS board member to any challenge or inquiry: they don’t need to consider it if it is not published in a scientific journal. De Harven’s response goes even further in saying that a plagiarism charge against claims published in marginal publications like JPANDS or on the Rethinking AIDS website must have a scientific sponsor to be valid. The same sentiment was expressed by Marco Ruggiero recently in a reply to our critique of Duesberg’s rehashed Medical Hypotheses paper:

All the considerations written by Chris Rawlins and Claus Jensen are interesting indeed. I have a suggestion; why don’t you publish them in a peer-reviewed scientific journal indexed in PubMed? Or, alternatively, why don’t you present them at some International Scientific Congress on AIDS? It is not difficult, I guarantee; Prof. Duesberg, Bauer and myself have done it hundreds of times. If you need an academic affiliation, I can easily provide you with a temporary one. Publishing will make your considerations much more valuable for the entire scientific community. (Ruggiero, Jan 2012)

Readers familiar with our post “PubMed Bagging with Bauer and Ruggiero” may be excused for thinking that this is voluntary self-satire, but rest assured there is nothing voluntary about it, Ruggiero truly believes it is a knock-out argument that a critique of an unpublished (or recently published at the time) paper has not appeared in a scientific journal.

To see how empty is de Harven’s and Ruggiero’s conceit one merely has to look at their response when the analysis or rebuttal does appear in a scientific publication. First de Harven on the same plagiarism charge:

- I was well aware about the fact that the PG had reviewed some data concerning endogenous viruses in the 90′s. But this was not their own work, from their own lab!!  They had reviewed OTHER PEOPLE’s WORK, and I don’t see why I should have included their reviews?  When I speak in my JAPS paper about HERVs and about circulating DNA, I carefully quoted Lower (77) and Anker (85) who are real molecular virologist/biologists, WORKING AT THE LAB BENCH!

What to do when the proof of one’s plagiarism fulfills the arbitrary criterion of having been published in a scientific journal? Easy, one simply raises the bar in an equally arbitrary manner. Now review articles don’t count, only the work of “real virologists/microbiologists WORKING AT THE LAB BENCH!” Once again we are reminded of Ruggiero’s boast that he is a real scientist because he works in a real lab while others “just talk” (Ruggiero has apparently forgotten that his proudest inspiration, post-modern philosopher and charlatan Jaques Derrida, also “just talked”), but even more so of Duesberg’s reply when Joyce Arthur asked him why he hadn’t replied to a published rebuttal of his Medical Hypotheses paper in the journal AIDS and Behavior.

The new Essex paper on “denialism” is, however, from without my professional expertise and published in a journal that deals with “behavior”.  Neither “denialism” nor “behavior” are within my current professional expertise.  Instead I am a scientist dealing with facts and hypotheses and theories.  Once the original scientific debate is settled in a scientific journal, I might, however, try to take a course on “denialism” and “behavior” in order to understand whether this is relevant to science. (Duesberg to Joyce Arthur Dec. 2011)

Duesberg is seemingly unaware that there is such a thing as a science of behaviour, at least as “hard” as his favourite hobby, epidemiology, that deals with facts and hypotheses and theories. But even if he were aware it surely wouldn’t qualify in his view, since science is something one does at the “LAB BENCH!”

The ignorance and conceit on display in these standard replies to anything perceived as being less than pure hero-worship is self-defeating for a variety of reasons, but chiefly because no dissident, per definition, is impressed with such answers, similar in every particular to the excuses given by the Orthodoxy for not engaging with critics. By using this line of argument Duesberg et al. self-identify as anti-dissident. They also self-identify as contemptible hypocrites since their own blogs and websites are full of complaints about the peer-review system, defences against allegations of practicing pseudoscience and of their own (lack of) credentials, the right to have their papers judged on the merits, calls for open debate in any forum, etc.

We have shown previously how the Rethinking AIDS board with Crowe as president, Duesberg as the chief scientist and Bob Leppo as the financial backer has become a perfect microcosm of the corrupt, interest-conflicted intertwining of money, science and politics they claim to oppose. With Ruggiero in the picture it has now also become a perfect microcosm of the members only cronyism that characterises the HIV/AIDS establishment. Ruggiero’s false boast about having done it “hundreds of times” notwithstanding, publishing dissenting papers about HIV and AIDS is nearly impossible even for those with permanent academic affiliations, impressive formal credentials and good connections. As Duesberg himself tells everybody who can be bothered listening, he tried several other journals, including the bottom-ranking JPANDS, before finally having to settle for the unlikely Italian Journal of Anatomy and Embryology (IJAE), which by strange coincidence happens to be published by Marco Ruggiero’s academic affiliation, the University of Firenze. By another strange coincidence, the “hundreds” of international scientific congresses on AIDS attended by Ruggiero, Bauer and Duesberg since Ruggiero became a board member were also Italian affairs if not directly hosted by Ruggiero’s university.

Significantly, all successful submissions for IJAE and scientific congresses (actually no more than a handful) by Bauer and Duesberg list Ruggiero’s students and co-workers from the University of Firenze as co-authors. Daniele Mandrioli and Ruggiero himself magically became distinguished “co-authors” on Duesberg’s latest paper, the earlier versions of which they had nothing to do with, by adding these three random Italian tidbits:

Almost identical figures have been reported recently for Italy, where AIDS is also still restricted to the original risk groups and paediatric AIDS is virtually non-existent (Ruggiero et al., 2009).

Similar non-correlations between mortality and prevalence of HIV were found in Italy. The Italian case is, however, based on actual data rather than on estimates (Ruggiero et al., 2009).

And a recent Italian study reported that the high toxicity of early anti-HIV treatment was responsible for the death of 2000 AIDS patients in 1997 (Ruggiero et al., 2009).

The co-authorship of other people on the list has left even less of a trace. And that is all quite in order. While it might occasion a quiet smile, one dissident should not begrudge another these “Trojan horses”, publishing in obscure journals, edited by friends and close colleagues, under laughable pretenses of relevance to anatomy and embryology, or the artificial ways of padding author lists and résumés. We all know that no other avenue is open, and the Orthodoxy sustains itself on this kind of mutual favours and back-slapping so why should dissidents deny themselves the opportunity when it arises? However, crowing about it in this way, ridiculously exaggerating one’s mainstream bona fides in order to mock or impress fellow dissidents once again reveals the mindset and the spirit of Rethinking AIDS as profoundly anti-dissident.

A little known fact, little known because it should not matter among dissidents, is that at least three of the Rethinking AIDS JPANDS publications, two by Bauer, one by Duesberg, were sent to the Perth Group for review. In the case of Duesberg’s paper the Perth Group referred JPANDS editor L. R. Huntoon to the critical analyses on the TIG site – ironically the same analyses Ruggiero believes are of no value because they haven’t been PubMed indexed. That alone, disregarding the Perth Group’s entire scientific corpus, would have been enough by Rethinking AIDS board standards to earn TIG members a co-authorship of the latest version of Duesberg’s paper. But the reality is that for dissidents to achieve “hundreds” of co-authorships the only important qualification at the moment is to be in Ruggiero’s and Duesberg’s good book.  That is the very definition of the corrupt mainstream cronyism Rethinking AIDS pretends to be opposed to.

Returning to de Harven, we readily see how the practice of quoting the Perth Group as authorities, even seeking their advice and opinion one moment only to turn around and mock them for not being real scientists the next, plays out. De Harven is seemingly oblivious to the fact that the 1993 paper by the Perth Group he thought was too amateurish to reference on the origin and nature of HIV DNA is the same paper he references as authoritative if not definitive on the origin of the HIV proteins:

The considerable difficulty in isolating and purifying HIV was recognized, as early as 1993, by Eleni Papadopulos et al., who correctly concluded that without successful HIV purification, the retroviral nature of the “HIV marker proteins” was most uncertain. Papadopulos emphasized that these proteins are most likely cellular, originating from the abundance of cell debris in poorly “purified” HIV samples.  (de Harven, JPANDS, 2010)

By applying his wholly arbitrary criteria of scientific validity in this wholly arbitrary manner to qualify and disqualify the Perth Group as circumstances dictate de Harven can now claim that Robin Weiss in 2008 was the first to point out that so-called endogenous retroviruses confound HIV research, because, although the Perth Group already explicitly reached that conclusion in 1993, they’re only real, quote-worthy scientists when it concerns the HIV proteins.

There is only one problem with this, nowhere in the cited paper do Weiss et al claim that HERVs have confounded HIV research. They do claim that HERVs are confounding factors for human retrovirus discovery, but nowhere do they claim that this applies equally to the already discovered HIV. We expect, however, that this is only a minor difficulty for de Harven, since to him the important thing is that he can quote a real lab bench scientist, even if the quote is made up.

Since de Harven now has credited the no doubt grateful Robin Weiss with the “new idea” that HERVs have confounded HIV research, what is his own contribution? According to himself it boils down to this:

the indisputably NEW IDEA in my paper is for having associated HERVs and circulating DNA, something the PG never alluded to

In other words, if the human genome is made up to any degree of HERVs a corresponding fraction of circulating human DNA will reflect this, and the viral load tests will pick it up. As has been pointed out to de Harven many times, he is indeed the first to present the “NEW IDEA” that the viral load tests detect retroviral DNA, since every “real lab bench scientist” stupidly insists that the viral load detects RNA rather than DNA. If de Harven could be persuaded to indulge all those scientists who perform viral load measurements on circulating endogenous RNA rather than DNA, he will be able to find plenty of references to prove that the association between HERVs and circulating RNA has long been assumed as a matter of fact. This 2006 paper, chosen at random, discusses the link between “HIV” infection and HERV expression as measured by the viral load test. It is hard to imagine how the paper could have been conceived and written if it were not established as a matter of fact that HERVs and circulating RNA are “associated”, and indeed that “HIV infection” and HERV expression are associated – although, according to de Harven, these researchers should not have been able to distinguish between HIV and HERV-K in their viral load tests.

Logically speaking, if the nucleic acid tests don’t pick up on a unique exogenous retrovirus, what could they possibly be picking up on but circulating cellular material? De Harven’s “NEW IDEA” is to point out that if you believe a part of the human genome consists of so-called HERVs, you naturally also believe that some of the cell-free cellular material will consist of such HERV fragments. If, like Dr. Maniotis, you correctly leave out the virus part of “retrovirus”, you will associate the viral load tests with circulating “retroids”. If, like the Perth Group, you don’t agree with calling these genomic elements viruses or retroids, then of course you will not explicitly associate HERVs with circulating RNA/DNA, you will most often simply call it cell-free cellular material. The point is almost too trivial to make, certainly too trivial to warrant a scientific paper based on it.

CLAUS JENSEN

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Professor Etienne de Harven: First among Plagiarists

We have talked often enough about the blatant plagiarism and history re-writing that seems to be Rethinking AIDS’s most important function these days, but among all the unabashed reinventors of the wheel that constitute its active board members Prof. Etienne de Harven deserves special distinction as indisputably the first among equals. His claim to originality is set forth in his article for the Journal of the American Physicians and Surgeons (JPANDS) called Human Endogenous Retroviruses and AIDS Research: Confusion, Consensus or Science? In connection with this article de Harven makes several related claims, which we have summarised below:

1. Nobody has come up with a satisfactory (alternative) explanation for the detection of “HIV”, especially via PCR, in some people’s blood.

2. Nobody has thought of linking the “HIV phenomena” to so-called endogenous retroviruses, only de Harven has had the scientific insight and imagination to perceive a connection.

3. Nobody has thought of linking Montagnier’s “HIV” EM to endogenous retroviruses.

4. Major claim: de Harven’s brand new dissident idea is that HIV research has been confounded by endogenous retroviruses.

In the introduction to the main topic of his JPANDS paper, the “HIV viral load” test, de Harven cites Eleopulos et al. 1993 as evidence that “the (HIV marker) proteins are most likely cellular, originating from the abundance of cell debris in poorly “purified” HIV samples.” But apparently de Harven has only read half of the paper he cites, otherwise he would surely have noticed the section “Genomic Investigations”, which begins thus:

At present it is generally accepted that “one of the most striking features that distinguishes retroviruses from all other animal viruses is the presence, in the chromosomes of normal uninfected cells, of genomes closely related to, or identical with, those of infectious viruses”80.

Depending on conditions, the provirus genome remains unexpressed or part or all of it may be expressed. The latter may or may not lead to the assembly of viral particles (endogenous retrovirus). 80  In other words, the finding of a viral genome (DNA) or even of RNA, antigens and antibodies to them, is not proof of the presence of infectious particles. Although most of the above findings are from animal experiments, at present, evidence exists that “The human genome carries DNA sequences related to endogenous retroviral genomes that are subdivided into families according to sequence homology. Some are present in only a few copies, whereas others are present in hundreds to thousands of copies”.133 Animal data also shows that new retroviruses may arise by (a) phenotypic mixing; (b) genetic recombination and deletion. When a cell contains two proviruses, progeny may be found that possess the genome of one but the structural proteins of either or both viruses present. Conversely, the RNA may be viral but at least some of the proteins may be cellular. In other instances, the particles do not have a genome at all, or one or more genes are missing (genetically defective viruses). The genetic mixing can be between viral genomes or between viral and cellular genes.80 134 According to distinguished retrovirologists such as Weiss and Temin, new retroviral genomes may arise by rearrangement of cellular DNA caused by many factors including pathogenic processes, a view that proposes retroviruses as an effect and not the cause of disease.135 136  The time and appearance of the viral genome “may be millions of years in germline cells and days in somatic cells”.136 In addition to the above, the retroviral replicative cycle “involves three distinct steps: reverse transcription, DNA polymerization, and the synthesis of RNA from a DNA template (transcription). Any errors made by the polymerase enzyme during the first and the third steps are not subjected to proof reading, the result being pronounced sequence variability”.137 Hence, as long ago as 1973, it was concluded that the above phenomena “will prove a stumbling block to any genetic analysis of RNA tumour viruses”138  (RNA tumour viruses=retrovirus). To date, the data on the HIV genome has not altered the above prediction and shows that many problems may exist with the use of the genomic studies in efforts to prove infection of AIDS patients with a unique exogenous retrovirus.

In this single passage the Perth Group not only express de Harven’s “new idea”, they anticipate and go well beyond his full argument and in much greater depth. The “stumbling block  to any genetic analyses of RNA tumor viruses” (so-called endogenous retroviral sequences in the human or animal genomes), which the Perth Group extends to difficulties with proving HIV infection in AIDS patients, is what de Harven clumsily rechristens as “the interference of HERVs in AIDS Research”.

For those who need more examples, here is what the Perth Group asked Peter Duesberg and all dissidents during the Continuum debate in 1995:

Reinhard Kurth, from the Paul-Ehrlich Institute in Germany, and his colleagues, reported that 70% of “HIV-positive patients”, compared to only 3% of blood donors, had antibodies which reacted with the retrovirus HTDV/HERV- K. However, HTDV/HERV-K is not a retrovirus which is present only in AIDS patients, that is, an exogenous retrovirus as HIV is said to be, but HTDV/HERV-K is an endogenous retrovirus or, as Kurth put it, a retrovirus present “in all of us”. How is it possible then to say, based just on an antibody test, that “Montagnier’s strain”, if one assumes Montagnier did isolate such a virus, is not another endogenous retrovirus generated by the conditions present in these patients? [This reference also contains a greatly expanded version of the Perth Group's 1993 discussion on the "HIV genome"]

Since de Harven introduces the Perth Group’s original idea, formulated in different ways in different contexts over the years, unattributed, and even specifically claims it is his own original contribution although he is well aware of the Perth Group’s work, this is plagiarism of the first water. If published under the auspices of a respectable institution, publication or organisation it would have very serious consequences. Needless to say this doesn’t apply to Rethinking AIDS or JPANDS.

De Harven’s biggest difficulty in the paper is explaining why, if “HIV” is a HERV, we are not all positive on the PCR tests, so he simply skips that part and instead muddies the water by informing the reader that:

Human plasma carries various amounts of circulating DNA. Suspected for a long time, this was first demonstrated by modern technologies in 1999, by P. Anker et al., in the blood of cancer patients. (de Harven)

As the title of the study cited by de Harven informs the attentive reader, it was tumour DNA in particular, not “various amounts of circulating DNA”, that was detected by Anker et al. But the question is what relevance does this have to the “HIV viral load”? De Harven continues:

Apoptosis and a large spectrum of infectious diseases are constant components of all clinical AIDS cases. Circulating DNA is expected, therefore, in the plasma of all symptomatic AIDS patients. (de Harven)

Circulating DNA is in fact expected in everybody, as de Harven has just informed us, although the quantity might be higher in cancer or AIDS patients, and the “HIV viral load”, which purports to measure RNA and not DNA, is detectable in the plasma of both symptomatic and asymptomatic HIV positives, so how can de Harven without further ado conclude that, “Retroviral sequences in plasma pellets (is) easily explained by the presence of variable amounts of circulating DNA”? Nowhere does de Harven say anything about possible qualitative differences in the circulating genetic material, instead it is time for another leap of logic:

(O)ne should not, however, expect that these nucleotide sequences would be identical in all cases. Quite to the contrary, since “nucleotide sequences that diverged from co-linearity with the typical retroviral genome (LTRgag-pol-env-LTR) considerably increase the number of HERV families,” the large number of HERV families resulting apparently from frequent recombinational deletions. Expected variations in the observed nucleotide sequences have, unfortunately, often been misinterpreted as an indication for a high rate of HIV mutations! It seems much more likely, however, that the numerous variations in the observed retroviral nucleotide sequences in circulating DNA reflect the large number of HERV families they originate from, and have nothing to do with presumed “mutations” of a hypothetical HIV. (de Harven)

In order to skirt the difficult issue of the “unique HIV genome” and why it is not present in all of us, de Harven simply decides that HIV is not a HERV, but any HERV; the “HIV viral load” detects retroviral sequences indiscriminately whether they belong to the same or even different families of HERVs. If this were the case it would follow that it has never occurred to a single out of the thousands of virologists who have been working with “HIV” that one retroviral sequence couldn’t be just as good as another when it comes to HIV testing. De Harven wants the reader to accept that the virologists who perform “HIV isolation” and who design the nucleic acid test kits use primers that will pick up on anything that’s remotely retroviral, be it DNA or RNA, endogenous or exogenous, from this or that HERV family.

Needless to say, de Harven doesn’t provide a shred of evidence for this claim, and to expose his conceit and the incompetence of an editor who prints this kind of unsubstantiated speculation one need only ask one question: If the virologists can’t tell the difference between “HIV” and the various HERV families that “confound AIDS research”, how do they distinguish between the different HERV families in the first place?  Or going back to the original difficulty, if the “HIV viral load” tests are not even specific to any one family of HERVs but react with all of them, why isn’t each and every one of us, or at least all who suffer from illnesses such as cancer, resoundingly positive?

To better understand how wafer thin is de Harven’s and Rethinking AIDS’s grasp of the substance matter, we invite the reader to read Bauer’s blog and especially the mini Q&A session following the post that touts Harven’s article in these optimistic words:

Not much if anything was known about human endogenous retroviruses (HERVs) at the beginning of the AIDS era. By now, a great deal has been found out, and some of it is directly relevant to various conundrums and controversies about HIV. In my opinion, recognition of the existence and characteristics of HERVs offers the possibility of resolving differing views among AIDS Rethinkers, as to whether HIV exists or whether it exists but is harmless. (Bauer)

Firstly, while human endogenous retroviruses is a fairly new field, animal retroviruses had been studied for decades, by Peter Duesberg among others, before the AIDS era. Secondly, the only HERV characteristics that matter in relation to de Harven’s article are that HERVs are 1. viruses 2. “retros” 3. endogenous 4. capable of producing particles 5. able to recombine. Points 1, 2, 3 and to some extent 4 can be learned simply from reading the name “endogenous retrovirus”. Point 5 is not a tautology, but of course it was well known by 1981.  Thus, apart from their putative existence in the human genome there is nothing in de Harven’s article about endogenous retroviruses that has not been well known for decades. Zero.

In the Comments thread, the central issue of the HIV genome and its origin was raised by Valerie McClain:

(Quoting Duesberg) “The existence of the retrovirus HIV predicts HIV DNA can be isolated from the chromosomal DNA of infected cells. The prediction has been confirmed as follows: Full length HIV-1 and HIV-2 DNAs have been prepared from virus-infected cells and cloned in bacterial plasmids.” Cloning in bacterial plasmids is a genetic engineering technique. Later in this article Duesberg states, “Thus HIV isolation based on molecular cloning exceeds the old standards defined as ‘Pasteur’ rules by Continuum.” (McClain)

Under ordinary circumstances we would expect Bauer to explain to McClain the exact reason why de Harven has ruled out that “”HIV” is an exogenous virus, but these are not ordinary circumstances:

Valerie:

I do now understand your point. Duesberg is (was?) universally agreed to be expert on retroviruses. Perhaps all of retrovirology used this same sense of “isolation”?

What you cite can still be interpreted in terms of HERVs, it seems to me. To prove exogenous HIV, one would have to show that this “isolation” could NOT be done on a given individual who later became infected which made such “isolation” possible. Since the epidemiolog of “HIV” tests shows that what is being detected is not infectious, either “HIV” is HERV-related or HERV-generated, or the “HIV” tests don’t detect what Duesberg was talking about, which seems unlikely. But I wish a molecular biologist would comment. (Bauer)

Bauer’s answer is as empty as de Harven’s article: First he excuses Duesberg’s deficient understanding of virus isolation by reminding us that Duesberg is an eminent expert in the field. In Bauer’s world eminent experts cannot be expected to be able to follow arguments based on simple logic or understand the meaning of words. Next he all but suggests that Duesberg is a proponent of the HERV theory of HIV, but, presumably because of his superior expertise in retrovirology, he doesn’t understand that what he says can be interpreted in terms of HERVs. Valerie McClain is citing from Duesberg’s second reply to the Continuum challenge about proof of the existence of exogenous HIV. According to Bauer, then, even when Duesberg specifically sets out to prove that HIV is not a HERV, he actually confirms it.

Since Bauer has just informed us that “a great deal has now been found out about HERVs”, the least one would expect is that he is aware that HERVs are not considered to be full length DNA genomes of functional retroviruses; if they were, they would not be described as “fossils’, “remnants”, “defective”. Even the (in)famous “Phoenix” paper from 2006 only claims to establish the theoretical possibility of functional HERVs in vivo:

Human Endogenous Retroviruses are expected to be the remnants of ancestral infections of primates by active retroviruses that have thereafter been transmitted in a Mendelian fashion. Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element, Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny. We also show that this element amplifies via an extracellular pathway involving reinfection, at variance with the non-LTR-retrotransposons (LINEs, SINEs) or LTR-retrotransposons, thus recapitulating ex vivo the molecular events responsible for its dissemination in the host genomes. We also show that in vitro recombinations among present-day human HERV-K (also known as ERVK) loci can similarly generate functional HERV-K elements, indicating that human cells still have the potential to produce infectious retroviruses.

Keeping this in mind here’s how Duesberg decribes “HIV” in McClain’s reference

HIV has been isolated by the most rigorous method science has to offer. An infectious DNA of 9.15 kilo bases (kb) has been cloned from the cells of HIV-antibody-positive persons, that – upon transfection – induces the synthesis of an unique retrovirus. This DNA “isolates” HIV from all cellular molecules, even from viral proteins and RNA. Having cloned infectious DNA of HIV is as much isolation of HIV as one could possibly get. The retrovirus encoded by this infectious DNA reacts with the same antibodies that cross-react with Montagnier’s global HIV standard, produced by immortal cell lines in many labs and companies around the world for the HIV-test. This confirms the existence of the retrovirus HIV. The uniqueness of HIV is confirmed by the detection of HIV-specific DNA sequences in the DNA of most antibody positive people. The same DNA is not found in uninfected humans.

If Bauer’s considered opinion is that these words are compatible with HIV being a HERV, and that with de Harven and himself as benevolent arbiters all differences between the Perth Group/Stefan Lanka and Duesberg could easily be resolved, why would there be a need for an unspecified molecular biologist to come along and help him out with the central questions? Why didn’t he simply ask de Harven, the author of the article, or Christian Fiala or Gordon Stewart, both credited by de Harven in the published article? They are all sitting on the same board, so it shouldn’t be too difficult.

The answer is this: The piece is plagiarised wholesale from the Perth Group; it is a watered down, distorted, shallow, incoherent reinvention of but one part of their comprehensive analysis, and it is perfectly natural that only the Perth Group themselves possess the depth of knowledge and research to answer all the difficult questions about their own work. Any former dean or professor knows this from experience, but they also know that the plagiarists cannot go to those they have plagiarised, so all they can do is wring their hands, wishing for a deus ex machina molecular biologist to happen along and save the day – when they are not pretending to be too busy and aloof to hear the questions.

Update: Above we asked, “if the “HIV viral load” tests are not even specific to any one family of HERVs, but react with all of them, why isn’t each and every one of us , or at least all who suffer from illnesses such as cancer, resoundingly positive?” De Harven has written a short paper on HIV PCR where the challenge is even more emphatic:

6% or more of the human genome has striking homology with retroviral genome, a fact that is well documented for more than a decade. So, PCR has no difficulty to recognize short retroviral-like sequences in these human chromatin samples (never twice the same, but never mind: it keeps mutating !!), and to amplify it 1000 or million times!  Bingo: this is HIV !!!!!!   NO: it is the amplification of endogenous retroviral sequences that are present in ALL OF US! It has NOTHING to do with the hypothetical presence of circulating retroviral particles! It has nothing to do with any “measurement” of the “viral load”.  By that method, WE ALL have some level of …”viral load”!!!  Really? Yes, but to save the establishment from too much embarrassment NO CONTROL, on you and me,  was ever made nor published!  Do you know the reference of one single paper in which a large group of “normal” individuals would have been studied for HIV “viral load” by PCR measurement? I don’t. (de Harven)

This is a valid point and we are sympathetic to it, but again whence derives de Harven’s certainty? There are in fact large groups of “normal” people who are continually being tested for “HIV” using nucleic acid testing. For instance, babies of HIV antibody positive mothers are likely to carry maternal antibodies for several months, so the PCR tests are considered more reliable than the antibody tests for infants. Not all infants, not even all African infants, test positive on PCR. Likewise, PCR is often used as part of the testing algorithm to confirm the positive antibody result in low risk groups.  It would help dissidents greatly if de Harven instead of making unsupported statements in his published papers would deal with specific questions like why are not all babies positive on the nucleic acid tests. Until he faces those challenges we can only conclude that de Harven once more has misunderstood and misapplied what he has misappropriated, namely the Perth Group’s argument that the nucleic acid tests are unspecific and correlate none too well with AIDS or the other “HIV” molecular markers.

CLAUS JENSEN

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PubMed-Bagging with Bauer and Ruggiero

 

[T]he Organizing Committee deserves a substantial credit for having accepted Rethinking AIDS as a legitimate association involved in the fight against AIDS. In fact, the Organization accepted the Italian member of the board of directors of Rethinking AIDS, Prof. Marco Ruggiero, as a qualified representative of the HIV/AIDS community and granted him free registration and access to all the events, including the sumptuous gala at the world famous Palazzo della Signoria seat of the Medici Family in Renaissance times. (Ruggiero/Crowe: The End of Dissent)

Ecco l’articolo tradotto in italiano

 

The latest post on Henry Bauer’s blog is introduced by this explanation of why an old affair has become newsworthy again:

The Italian Journal of Anatomy and Embryology has now published (volume 116 #1, supplement, 2011, p. 157) the abstract of the poster shown in AIDS Rethinking presented in Mainstream Conferences (posted on 2011/09/29). The mainstream literature now contains this summary of crucial deficiencies of HIV/AIDS theory, in a journal abstracted by PubMed.

It is indeed cause for celebration whenever dissidents get to say their piece in any public forum, but as Bauer informs us, we have already celebrated with him the inclusion of this paper in a mainstream forum, so what’s the significance of achieving a reference in PubMed in this sort of roundabout way? The honest answer is very little – apart from it being a feather in the author’s cap.

In light of this, the question becomes why does Bauer pretend that there is anything new or extraordinary in achieving a PubMed reference? We have previously documented how he and his Rethinking AIDS cronies are busy rewriting the history of dissidence to place themselves at the centre of it, and this could be seen as simply part of the effort to leave one’s scent on as many  fire hydrants as possible in the battle for dissident territory. But there seems to be something even more fundamental at play.  We have commented several times on  Rethinking AIDS’s increasing eagerness to become accepted by or even be part of the Mainstream. Their struggle to gain access to polite society  has led them to declare the “End of Dissent”, to identify themselves as disciples of Luc Montagnier, and even to support the existence of a proven Human Immunodeficiency Virus. Especially since the Duesberg et al. and Ruggiero et al. papers were retracted by Medical Hypotheses  we have seen these victory dances every time Rethinking AIDS Board members manage to get anything published, no matter how inane.

As Bauer’s latest post shows,  bagging mainstream references has become an end in itself, a kind of credit convertible into dissident capital. The metaphor prompts the question, how is that “capital” expended?  A couple of  recent examples are revealing. When asked recently by a third party  whether he is closer to Peter Duesberg, to Henry Bauer or to the Perth Group on virus isolation, Marco Ruggiero offered the following “clarification”:

I agree with Prof. Duesberg and Bauer. However, I have little interest in metaphysical retrovirology. I run a laboratory and I do research;
many others just talk. (Ruggiero email, Oct 2011)

In other words, the Perth Group are not real scientists, they “just talk”  and should therefore be dismissed out of hand. Profs. Duesberg and Bauer, on the other hand, are real researchers (even if none of them has worked with “HIV”), which means that Ruggiero automatically agrees with both their mutually exclusive positions. If the reader finds this kind of defensive snobbery familiar, it’s because it’s the core argument used by the mainstream against all AIDS dissidents.  As we’ve pointed out in a previous post, the self-congratulatory list of journals, organisations and scientific celebrities that now “accept dissent” that gushed triumphantly from Ruggiero’s (and Crowe’s) keyboard on the occasion of the Italian Conference on AIDS and Retroviruses in Firenze, 2011 did indeed mark the “End of Dissent” as far as Ruggiero and RA are concerned. They are now openly anti-dissent and even quicker than the establishment apologists to use their mainstream credentials, real or imagined, as a club to beat dissenters with.

The recent examples aren’t confined to Ruggierio. When Bauer recently was made aware that another blogger had commented on one of his posts, his knee-jerk response was:

Since that blogger is anonymous, there’s no way to discover whether he or she has any of the background called for if one wishes to be a pundit about scientific matter. (…) To compare the credentials of “Orac” to mine, have a look at my vita, at the books and articles I’ve written, and particularly the uniformly positive reviews of my books about science and pseudoscience. (Bauer, Nov 2011)

Bauer shares Ruggiero’s sentiments: if someone cannot match his credentials, and on top of that doesn’t agree with him, why should he bother with what they have to say? (“Orac” didn’t have anything to say, in fact his argument against Bauer was similar to Bauer’s argument against him, but Bauer’s readers would never know).

In another recent email exchange,  Duesberg, Crowe, Bauer and Ruggiero expressed their scientific opinions on the Perth Group’s latest Statement in this manner:  ”bizarre”, “sad”, “It’s neither science nor even conventional politics. Are they getting old?”. The last comment came from Duesberg, so we gather that his lab research and the fine company he keeps has made him an expert not only on the difference between science and politics, but also on the fine distinction between conventional and unconventional politics. Here Rethinking Aids’s favourite  maverick mocks the Perth Group for not being “conventional” in full agreement with Rethinking AIDS’s new brand of Respectable Rethinking. Characteristically, for all the condescension and smugness in the eight-mail exchange, there were no specifics about what the distinguished researchers found “sad”, “bizarre” or generally unscientific.  There is not even the faintest hint that any of them had  read and considered the statement they were commenting on, but the message is clear enough:  The conventional politicians and scientists of Rethinking AIDS, in lofty pursuit of PubMed trophies, consider themselves  above  engaging with the group that represents the position of most AIDS rethinkers.

At this point those  dissidents who still believe in dealing with the substance of people’s arguments rather than just their publication record or the number of stars on their shoulder might ask what the  ”summary of crucial deficiencies in the HIV/AIDS theory” that Bauer and Ruggiero managed to get referenced in PubMed consists of.  The answer is none. They list a couple of things (basically Bauer’s favourites about racial disparities in HIV prevalence) the authors find paradoxical about “HIV” epidemiology.  They then proceed to offer the explanation that these “deficiencies”  are actually due to:

weaknesses  in  HIV  testing,  which  are  the  probable  reason  for at  least  some  of  the  troubling  conundrums  and  mutually  contradictory  data  that seem inexplicable (Bauer/ Ruggiero)

If Bauer and Ruggiero’s theory is  correct it means that the issues they list are unrelated to any deficiencies in the HIV/AIDS theory. Technically flawed tests are just that, technical problems that can never translate into deficient theory, and if the “deficiencies in HIV/AIDS theory” summarised by the authors are so easily explained away they can hardly be “crucial”. In fact, if the reader truly wishes to find PubMed-abstracted summaries of deficiencies in the HIV/AIDS theory based on epidemiology, simply do a search on Peter Duesberg. Similarly, if one wants to find PubMed-abstracted summaries (and much more) of  ”weaknesses in ‘HIV’ testing” in Africa and elsewhere, one can do so here or here or here or here or here or a score of similar references.

Bauer and Ruggiero add nothing but fog to these accounts. For instance, their summary begins by stating the fundamental problem that there is “no gold standard HIV test”, and this immediately begs the first question: Why talk of a gold standard test when it is the gold standard itself that is missing? The authors even go on to claim that if such a test were in existence false-positives (contradictory test results) would not occur, which is patently absurd. The distinguished research scientists have managed to confuse gold standard and gold standard test to produce almost inextricable nonsense from the outset:

This situation has been particularly troublesome in the case of HIV, because there is no “gold standard” HIV test and the typically quantitated measure, CD4, varies widely  for  a  variety  of  reasons  that  have  nothing  to  do  with  HIV  infection.  For example, a person pronounced HIV-positive after having some vaccinations became HIV-negative  again  after  a  time,  something  that  is  not  regarded  as  possible  if  HIV- positive  denotes  definitely  active  infection,  as  is  commonly  assumed. (Bauer/Ruggiero)

One should be clear that all talk of a gold standard test involves an infinite regress. Let us say that a test that detects a certain hormone is the gold standard test of pregnancy because out of  1 million cases of pregnancy it was positive every single time, and in 1 million control cases of no pregnancy it was negative every single time. We would then need to ask how it was established that there really was a pregnancy in the positive cases and none in the negative cases to validate the hormone test.  Perhaps the answer would be that within 9 months or less we were able to touch and look at a newborn baby. It is reasonable to say that the “touch and look ” test trumps the hormone marker test, but it is also quite reasonable to ask how we know that our senses are not betraying us in any number of those cases. The answer might be that our observations are confirmed by other people’s observations and by instruments that are known not to fail, for example those used in the aforementioned hormone marker test. And so on in an infinite regress or infinite circle of mutually confirmatory tests. That is why Cowen and Weiss, Bauer’s supreme reference in most of his papers, tell us that the gold standard  is ultimately a matter of consensus:

Gold Standard (Reference Standard) A definitive means of categorisation, widely accepted by experts in the field, for absolutely defining the presence or absence of a condition (such as HIV infection).  (Cowen and Weiss. See Eleopulos’s PS to her peer review of a Bauer paper for JPANDS)

The problem therefore is not lack of a gold standard test, that can be solved merely by sitting down and “widely accept” that a given test or test algorithm is the gold standard. The problem is that the most fundamental agreed upon gold standard test,  virus isolation as described by the Perth Group in their papers on the subject as well as most virology textbooks, has not been achieved. In short, the fundamental problem is not the missing test but the missing virus, and Ruggiero/Bauer in just a few lines manage to completely obscure this simple point.

As Wikipedia explains, the ideal gold standard test is 100% correct 100% of the time in accordance with all consensus and all confirmatory testing, so what Bauer and Ruggiero are expressing when they claim that a false positive result could not occur if there existed a gold standard test (and assuming that test was used as reference test every time) is either a tautology (the test is considered correct by definition as established by consensus), or by gold standard test they mean classic virus isolation, the one test accepted even by dissidents.

However, Wikipedia also calls the gold standard test hypothetical in most cases, because the agreed upon gold standard test can occasionally be wrong or produce contradictory results in practice. In either scenario contradictory test results, with the same test or with different tests, have nothing to do with whether a gold standard is in existence or not.  If virus isolation were the gold standard would Western Blot and ELISA cease to produce false positives? Of course not. It would be possible to make them extremely accurate, but there is no guarantee it  would make problems like cross-reacting antibodies disappear.  If the contradictory results  occur on the same test, gold standard or not, it would either be because of a flaw in the particular test kit/procedure or because the object of the test truly has disappeared.  Why would a gold standard test be inherently immune to either of these possibilities if the present tests aren’t?

One could object that this is what Ruggiero and Bauer really want to say, and that they are cleverly undermining the idea that “HIV” infection is necessarily permanent. Unfortunately, if that is what they are trying to do it is far from clever.  First of all, what does the issue of permanence of HIV infection have to do with the performance of the tests and whether there is a gold standard? There is no connection. In their anecdotal example of a friend who tested positive after receiving vaccinations, but later negative there are two possibilities:

1. The HIV infection was transient and the test correctly detected HIV’s presence and later absence.

2. This was a false positive brought on by the vaccination or other factors unrelated to HIV, and the follow-up testing correctly identified this as a false positive.

In either case the physician will correctly rule in the end that there is no cause for concern, so what exactly is Ruggiero’s and Bauer’s problem? Perhaps they prefer a different formulation:

1. The tests have technical difficulties with cross-reactive antibodies that are not specific to HIV, especially in places like Africa.

This is not news to any of the HIV experts. The only thing that could be of interest is if there were no (proof of) HIV, and all antibody reactions therefore must be considered unrelated to it.

2.  HIV was really there and now it’s gone (Montagnier HON), but the tests still pick it up.

If that is the case it means there is a real virus, that it has been isolated, and that its proteins and genetic sequence are known. In other words, there is a gold standard for the HIV tests.  This is in fact (by far the most expert) co-author  Ruggiero’s express opinion, and he even rejects the notion that the existence of a gold standard test would mean that the risk of false positives is eliminated:

Any test, by definition, cannot be 100% accurate. Specificity and sensitivity often are inversely related; therefore un-specific diagnoses of HIV-positivity are likely to occur as with any other test. In general, however, once such problems have been resolved, I would say that in the presence of confirmed antibodies and detection of the so-called viral load (although often over-estimated), I would say that an encounter with the virus has occurred. (Ruggiero to Celia  Farber in “Over the Rainbow”)

If by the careful formulation “encounter with the virus has occurred” Ruggiero wants to leave open the possibility that the infecting retrovirus was defeated and eradicated, the issue of real interest would be to know how this is possible, and how it is possible for the eradicated virus to leave antibodies and genetic material behind for the various “HIV” tests to pick up indefinitely. If this is Ruggiero’s and/or Bauer’s true position, why haven’t they written a truly original paper on their revolutionary discovery for PubMed  instead of constructing elaborate webs of almost impenetrable self-contradictions?

A final question is how Bauer and Ruggiero got this mishmash past peer reviewers and editors. Even if the finer points of “HIV” antibody testing are lost on the Italian Journal of Anatomy and Embryology, how could they fail to notice that the justifying premise for writing about it in an article on dissection for anatomy students is completely nonsensical?

An important  consequence  of  deficient  information  about  HIV  epidemiology  is  that  students  of anatomy may fear risking possible infection in dissection laboratories when the actual risk  is  negligible  even  in  respect  to  anonymous  cadavers  in  South Africa where the supposed  incidence  of  HIV  is  particularly  high. (Ruggiero/Bauer)

Firstly, how can the authors know the risk is negligible in various contingent circumstances if there is no reliable HIV test?  Secondly, vague speculations as to how many of their cadavers might test false and true positive based on indirect evidence from epidemiology are hardly relevant or reassuring to the anatomy students. If fear is born of ignorance, how could it possibly allay that fear to introduce yet more confusion and uncertainty concerning “HIV”? After reading the Bauer/Ruggiero article the students have to worry about the real number of countrywide infections, including their own status, being unknown and inherently unknowable, whereas all the epidemiology they previously needed to care about was how many accidental, real HIV infections resulting in AIDS cases have actually occurred during dissection, based on those state of the art test algorithms that at least one of the authors considers quite satisfactory. What could be more reassuring than a couple of paragraphs pointing this out if it were really unknown to the, according to Bauer and Ruggiero, perpetually terrified anatomy students?

CLAUS JENSEN

Ecco l’articolo tradotto in italiano: http://bit.ly/ygVOKR

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Discrepancy between Gender-Specific HIV Prevalence and Gender-Specific AIDS Mortality in South African Statistics disprove HIV > AIDS Theory (Duesberg vs. Chigwedere Part IV)

When Duesberg’s answer to  Chigwedere et al Estimating the Lost Benefits of Antiretroviral Drug Use in South Africa appeared in Medical Hypotheses we published  three critical analyses, one of Duesberg et al, one examining the calculations behind Chigwedere’s ARV treatment benefit estimate and one analysis of the evidence for a steep rise in child mortality caused by a new pathogenic agent. In the meantime Chigwedere and Essex published their own reply to  Duesberg, called AIDS Denialism and Public Health Practice.  In this article, the fourth part in our series about Chigwedere vs. Duesberg,  we will analyse Groenewald et al., one of Chigwedere’s key references, and show: 1. that it cannot be cited as proof of any aspect of the HIV theory of AIDS because it assumes that theory as a basic premise. 2. that it is powerful disproof of the HIV theory of AIDS because it reveals a glaring discrepancy between gender-specific HIV prevalence and gender-specific AIDS mortality in South African HIV/AIDS statistics.

Chigwedere and Essex’s second article rebutting Duesberg’s unpublished reply to their first political attack is similar to it in many ways. It is characteristically shallow and prefers to bombard the reader with a bewildering multitude of hard-to-penetrate references rather than performing meaningful analysis. It is therefore important to identify the relevant points in dispute. The critical assertion in Duesberg et al. is the following:

South African statistics have recorded only about 1 ‘‘HIV death” per 1000 HIV-positives per year (or 12,000 ‘‘HIV-deaths” among 12 million HIV antibody-positives) from 2000 to 2005.  (Duesberg et al)

Chigwedere et al. answered the following way:

The second part of the argument quotes Statistics South Africa, which recorded an average of 12,000 deaths per year in South Africa between 1997 and 2006 [3]. The shortfall is that these data are ‘‘Findings from Death Notification [118].’’ First, as explained by surveillance experts, ‘‘In resource-poor countries with underdeveloped health infrastructures, reports of AIDS or HIV cases are usually not complete enough to be considered reliable measures of the scope of the epidemic [119]’’. This simply means that the death notification system in South Africa had/has much underreporting. Indeed, the ‘‘former so-called independent homelands of Transkei, Boputhatswana, Venda and Ciskei (TBVC) were not included in the reporting system until 1994’’ when the reporting system began centralization, and a new death certificate was introduced in 1998 to improve reporting [120]. The second shortfall is that of misclassification of deaths. AIDS patients die of the resulting  opportunistic infections and cancers, and these immediate causes of death are often recorded without noting the underlying acquired immunodeficiency. According to the Medical Research Council (SA), up to 61% of HIV deaths are misclassified and the majority of them are recorded as tuberculosis and lower respiratory tract infections, which become the leading causes of death [120].7 It is apparent that Duesberg selected highly deficient statistics. (Chigwedere et al.)

We have previously shown that Duesberg et al. did indeed select deficient statistics to support their Passenger Virus theory. Duesberg was silent in the face of Chigwedere and Essex’s rebuttal, but co-author Henry Bauer addressed the issue indirectly in Galletti et al. and later in a blog post published in Jan 2011 called Picking cherries in South Africa - just as he had previously published a critique of Chigwedere’s first paper on his blog anticipating to some extent the approach in our first analysis. But as was the case with that effort Galletti et al. and “Picking cherries in South Africa” are sketchy arguments, and as a result the hard questions are never dealt with satisfactorily.  Consider for instance Bauer’s facile claim that the UNAIDS statistics have been “officially” debunked:

For some reason, the professionals at South Africa Statistics have been unmoved by this nonsense [Huge number of AIDS deaths]. Their latest published report on “Mortality and causes of death in South Africa, 2008: Findings from death notification” (P0309.3, released 18 November 2010) notes that the completion of reporting of deaths has been at around 80%, and that deaths from “AIDS” or “HIV disease” were a little over 15,000 in 2008, ranking 7th among causes of death, responsible for just 2.5% of all deaths. The UNAIDS model is once more officially declared to be wrong by a factor of 20 or so. (Bauer)

A report whose title specifies that it confines itself to reporting  “Findings from death notification” can hardly be taken as conclusive proof of, or even addressing the validity of the UNAIDS models. Those are different things and pretending otherwise is not going to impress an audience that has read Chigwedere and Essex’s well-referenced paper.

Bauer further cites Rian Malan on the continual down-revision of South African AIDS mortality to conclude that the ASSA model used to calculate the numbers is “thoroughly discredited”. But again, revised estimates discredit only the old estimates, not the current ones.  It should also be noted that Bauer, still citing Rian Malan, includes instances where not only AIDS deaths but HIV prevalence modeling was revealed as overestimations:

Malan also cited computer-modeled estimates of 9.5% “HIV-positive” for college students at Rand Afrikaans University when a large sample of them (nearly 1200) tested poz at only 1.1%; and a computer-modeled estimate of bank employees at 12% when actual testing of 29,000 employees revealed a rate of only 3%. The model is thoroughly discredited, in other words. (Bauer)

It is not clear how those estimates were arrived at, but Duesberg et al. used the huge disconnect between a 25%-30% HIV prevalence and 12,000 annual AIDS deaths to argue that HIV is not responsible for those deaths. If in fact HIV prevalence is overestimated, it only means that HIV prevalence and registered AIDS deaths match much better than Bauer/Duesberg pretend they do, which in turn means that their own statistical argument for HIV being harmless is also “thoroughly discredited”.  Even the none too bright Chigwedere and Essex know how to exploit  this inherent contradiction in Duesberg’s/Bauer’s argument :

The extreme end of the argument is to suppose that Duesberg’s low statistics of about 12,000 AIDS deaths per year were correct-that would translate to a total of 72,000 deaths from 2000 to 2005, and this would still enable a calculation of the number of persons that could have been treated using ARVs had Mbeki not obstructed, 24,000 lives if we assume a third of them would have been treated. This is not a small number of people to let die because of AIDS denialism. (Chigwedere/Essex)

It should be clear from this that sweeping epidemiomological arguments cannot settle the issue in favour of Duesberg et al. At some point one has to get down to the nitty-gritty of examining the specific references cited by Chigwedere and Essex, instead of chasing the red cloth of population curves and adjustable HIV/ AIDS estimates or accusing each other of cherry-picking, but Bauer stays the course over shallow waters in Galletti et al.:

The director of Statistics South Africa, Lehohla (2005; cited in Galletti & Bauer) has explicated the errors committed by those who rely on the UNAIDS models, for example by using long chains of inferences based indirectly on a host of doubtful claims that jump to farfetched conclusions based on changes in the age distributions of deaths and ignoring rises in political and criminal violence that account for those changes. By contrast, Chigwedere and other mainstream doom-purveyors have simply cherry-picked the invalid UNAIDS numbers and ignored the official Statistics South Africa reports. Those who attempted to defend the UNAIDS numbers coould only assert, without a shadow of evidence, that causes of death must have been misreported to the extent of almost half of all deaths; yet they have not even attempted to show how or why Statistics South African is wrong about its estimate of 80% completeness of counts and accuracy of reporting. (Bauer)

The reference for the categorical statement that political and criminal violence accounts for all changes in age distribution of deaths is South Africa’s Statistician General JP Lehohla. The only problem is that Lehohla says nothing of the kind.  He mentions unnatural deaths  (not political and criminal violence, which was decreasing) as one factor that could have impacted the year 2000 death rates in the 15-49 age group, but he does not suggest that they can explain the rise in AIDS indicator diseases such as tuberculosis and pneumonia. We are not dismissive of Bauer’s point as  part of a larger argument, but  the impressive numbers for unnatural deaths are all from 1996, well before HIV/AIDS is supposed to have impacted South Africa to an appreciable degree. All post-1997 reports from Lehohla’s Statistics South Africa (the report Bauer reads as gospel on AIDS deaths) show a steady or decreasing level of unnatural deaths and increasing levels of AIDS indicator diseases.

All of this brings us back to Chigwedere and Essex’s key reference 7 cited above for the 61%  misclassified HIV deaths. It is a paper by Groenewald et al. from 2005 entitled Identifying Deaths from AIDS in South Africa and it deals specifically with the issues of age-specific rise in AIDS indicator diseases and erroneous death certificates. It is in fact the “shadow of evidence” Bauer repeatedly claims does not exist although it features prominently in Chigwedere’s rebuttal of Duesberg et al. We will therefore place our hand on the lever and examine it in detail.

The first thing we learn from Groenewald et al. is how easy it is to make the numbers of AIDS deaths match up with the official HIV/AIDS estimates when one accepts there is such a thing as an HIV-related AIDS death. Groenewald et al. looked at the age distribution of the deaths determined as HIV-related, (the 12,000 annual AIDS deaths accepted by Duesberg et al.) and found a distinct age pattern. They then looked at all deaths in those same age groups and found that there was significant rise in mortality in the HIV era over and above what could be expected (excess mortality) due to recognised AIDS indicator diseases:

Methods: (…) The difference in the age-specific death rates for these two periods was examined to identify conditions where there was a noticeable increase in mortality following the same age pattern as the HIV deaths, thus likely to be misclassified AIDS deaths.

Results: The increase in the age-specific death rates for HIV-related deaths showed a distinct age pattern, which has been observed elsewhere. Out of the 22 potential causes of death investigated, there were nine that increased in the same distinct age pattern (tuberculosis, pneumonia, diarrhoea, meningitis, other respiratory disease, non-infective gastroenteritis, other infectious and parasitic diseases, deficiency anaemias and protein energy malnutrition) and could be considered AIDS-related conditions. The increase in these conditions accounted for 61% of the total deaths related to HIV/AIDS. When added to the deaths classified as HIV-related on the death certificate, the total accounts for 93% of the ASSA2000 model estimates of the number of AIDS deaths in 2000 (Groenewald)

It is a very reasonable assumption that the same agent, HIV, is responsible for the excess deaths where all three  correlates, HIV-related ages of death, HIV-related indicator disease and excess mortality, converge.  If the objection is raised as to what makes certain ages and certain diseases HIV-related, the answer is the HIV test. If one accepts the validity of the HIV tests even in principle, one must also accept that there are HIV-related ages of death and HIV-related causes of death.

However, Groenewald’s unquestioning acceptance of  the validity of the HIV > AIDS hypothesis presents a problem for Chigwedere et al. For example, Groenewald et al. felt free to consider not only excess mortality from recognised AIDS indicator diseases, but even non-AIDS indicator diseases in order to arrive at the desired figure:

Based on the literature, AIDS indicator conditions, including tuberculosis, pneumonia, diarrhoea, meningitis, wasting, septicaemia, lymphoma, cervical cancer, candidiasis, cryptococcosus and other opportunistic infections, were selected [11,13]. Clinical and autopsy surveys suggested that myocarditis (I40) and cardiomyopathy (I42) [14] should also be considered potential candidates for investigation as HIV-related deaths. On the basis of experience in Zimbabwe, which suggested that many HIV deaths were misclassified to malaria [15], malaria was also investigated. Maternal deaths were also selected on the basis of the most recent confidential inquiry into maternal deaths, which showed that the proportion of deaths from non-pregnancy-related infections (mainly AIDS) had increased dramatically between 1998 and 1999-2001 [16]. Kaposi’s sarcoma (C46) was added to the HIV-related deaths (B20-B24) as the 1985 Bangui definition for AIDS considered the presence of Kaposi’s sarcoma as sufficient for the diagnosis of AIDS for surveillance purposes [11]. Causes of death with no known association with AIDS, which had shown a marked rise during this period, were also investigated to ascertain whether this rise could be attributed to AIDS.

Groenewald et al. are to be applauded for their candidness, less so Chigwedere et al.: the Bangui definition, reports from other countries, autopsy surveys, causes of death with no known association with AIDS, everything but the kitchen sink is thrown into the mix. The authors feel they can pick and choose freely because they assume in advance that the excess mortality in the designated age groups is due to HIV. Since this is the claim in dispute, it should be obvious that Groenewald et al cannot be cited by Chigwedere and Essex as proving it.

It should also be emphasised that using  this method Groenewald et al. can make the numbers fit almost any ASSA estimate by picking and choosing between the initial 22 conditions considered. If, for example, the estimate is revised downwards, Groenewald et al. can decide that meningitis isn’t a reliable AIDS indicator disease in South Africa and scrap it partly or in full at their discretion. But far more importantly, this also means that where rising death rates do NOT match the age pattern the authors are looking for or the figures they are trying to approximate they have no problem attributing excess deaths to causes other than HIV. One example they give is melanoma, which had increased to almost 6 times previous levels around the age of 55. Had the peak occurred at age 35, the authors would likely have attributed it to HIV, but since the peak occurs at 55 the authors are quite happy attributing it to other causes. This illustrates nicely how empirical observation is made to fit theory instead of the other way round.

However, Groenewald et al. have a much bigger problem on their hands than mere cherry-picking. Since HIV prevalence is the only variable considered as a cause of excess deaths in the chosen age categories, it follows that excess mortality should track HIV prevalence faithfully. But in  Figure 1 we see that male mortality overtakes female mortality at age 35 despite the fact that female HIV prevalence is much higher than male prevalence for almost all age groups. Male HIV prevalence overtakes female prevalence briefly around age 35, but females are decisively back in the lead around age 40, so it cannot explain how the male HIV-related death rate can get in front and stay there.

Further, if we compare the 2002 curves with 1996, before the excess, HIV-related deaths supposedly kicked in, there is no age group for which the gender distribution of mortality has changed appreciably in the 6 years AIDS is suppposed to have exploded.  One would expect to see statistically significant divergence in the female to male ratio for at least some age groups but none is apparent, the 1996 and 2002 curves faithfully track each other in terms of female to male ratio.

The point is perhaps clearer if we move to Groenewald’s breakdown of actual numbers in Table 2, where he estimates that the overall difference between female and male AIDS mortality is approx. 6,000 in the adult category. This means that AIDS mortality has hit the sexes in almost equal measure despite HIV prevalence being much higher among females. How is that possible?

To give us a sense of the lopsided impact of HIV prevalence on women Groenewald cites the 26.5% prevalence rate at antenatal clinics, a good indicator of HIV prevalence among sexually active females. This is on background of an overall prevalence rate of 11.4%, which means that male prevalence must be significantly lower than 11.4%. Depending on how we cut it the ASSA-sanctioned difference between the sexes in adult HIV prevalence comes out at around 2:3 across all sexually active age groups. Assuming that HIV is the cause of AIDS, a 2:3 ratio between males and females means that the mortality figures Groenewald is operating with should be 72,000 female AIDS deaths to 48,000 male AIDS deaths. In other words, if AIDS mortality really tracked HIV prevalence the difference between male and female AIDS mortality in Table 2 would be somewhere around 24,000, 4 times higher than the 6,000 Groenewald arrives at. Thus the discrepancy between gender-specific HIV prevalence and gender-specific mortality alone should have led Groenewald to conclude that HIV is not a major cause of the gender-specific excess death rates in South Africa.

This problem is not unique to Groenewald; all South African gender-specific HIV prevalence statistics are contradicted by the corresponding gender-specific AIDS mortality, and we hope to be able to present a more comprehensive study in the near future, but here we emphasise that the discrepancy is intrinsic to the assumptions and calculations used to estimate the South African HIV/AIDS epidemic. Groenewald set out specifically to make HIV prevalence and AIDS death estimates match up any way he could. We allowed him all the room to manoeuver he wanted and still the numbers conclusively contradict the basic assumption they were meant to prove: that HIV is the cause of AIDS.  This is devastating to Chigwedere et al., who reference Groenewald as the best evidence they have that AIDS deaths in South Africa track HIV prevalence.

CLAUS JENSEN

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Lessons in Dissent

Revolution is not a dinner party, not an essay, nor a painting, nor a piece of embroidery; it cannot be advanced softly, gradually, carefully, considerately, respectfully, politely, plainly and modestly. – Mao Tse-Tung

One of the biggest problems with HIV/AIDS dissidence is that many who call themselves dissidents, including many who would like to believe they are politically sophisticated, are almost completely ignorant of revolutionary theory. After all this time and after all we have written  in all kinds of styles for all kinds of tastes, we still get comments like the one below:

I recognise the spreading nuances within RA and it is annoying that they carry on oblivious to the oddities they made themselves, but still it seems like PG has more of a grudge against RA than AIDS Inc.  Apparently Anthony got mad at Christine Johnson for wanting to remain neutral between RA and PG.  She might have joined PG if it had not been for him.  That’s the way it seems. (Received Oct 27, 2011)

[NOTE! The author of this message has asked us to make clear that when using the words "oddities" he refers to theories not personalities. We interpreted it as a comment on theories rather than individuals and believe our answer reflects that]

Our answer to dissidents in general:

If you want to be considered more than a joke who has chosen to dissent because it justifies not getting a real job, there are some fundamental things you should know by now. One of them is that dissidents will always be destructive, disruptive, bad-mannered, foul-smelling, and holding “more of a grudge”. It is intrinsic to dissidence if you’d care to stop and reflect just one second:

Dissidents are pitted against the status quo, which necessarily means disrupting and destroying everything that has its orderly functioning within the status quo. In this case Rethinking AIDS represents the status quo, entrenched power, as much as AIDS Inc. does, and the Perth Group are the dissidents.

Those already in power benefit from conciliation, hence they almost always advocate it, at least out of one side of their mouths, while their money, their media and their political influence are put to work subverting, slandering, co-opting and destroying the revolution, as are their police and the full force of their laws, with batons, pepper spray, searches, permanent surveillance and random arrests among the powerless.

Conciliation means keeping the staus quo that is inherently biased in favour of Power and against dissidents. Therefore those in power ALWAYS, and almost always successfully, assume the role of the reasonable compromise-seeking grown-ups and cast the dissidents as immature, unrealistic, ignorant. With their boots on the dissident’s neck they will tell him, “You are free to dissent and that shows how great and tolerant our democracy is, but be civil about it, follow the procedures that are built into our fine system of governance, that’s the right way, the responsible way to go about it.”

If you follow the Occupy Wall Street protests, as any serious dissident should because that is where the trenches are dug in the Western world at this point in time, you will have seen this dynamic being played out real time. Were you fooled by Wall Street’s own President Obama for one second?

Those in power control the propaganda machinery aka the mainstream media, thus the day-to-day narrative. Your own President Crowe has taken over the Rethinking ADS initiative, the Hivaidsparadigm forum and now the Rethinking Facebook forum by force, at least some of it while you were watching, uninvolved. Were you  fooled by this president for one second?

Internal house-cleaning is always more vicious than the battle against the external foe. That is because the enemy within is the most dangerous. If you allow him to subvert you it will be impossible to even begin battling the enemy without.  The Parenzee case provides the most vivid illustration of this truth imaginable.

Now, Christine Johnson is supposedly an intelligent woman, if she really made her decision in this matter of untold historical consequence based on whether “Anthony got mad at her”, what does that tell you about her? There is no such thing as “neutral”. Neutral is a weasel word for unprincipled, siding with Power.

What does it tell you about yourself when you say: “Yeah it’s kinda annoying, I guess, when the organisation that claims to represent us all make oddities of themselves – make oddities of us all – however, if only Anthony hadn’t become mad at Christine Johnson everything might be different, at least that’s how it appears to me”?

What does it tell you about yourself when in one mail you tell me you can’t be bothered getting involved and in the next you tell me how things appear to the uninvolved and the unreflective? It tells me that you should read the Mao quote a hundred times over before calling yourself a dissident again.

 

CLAUS JENSEN

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Rethinking AIDS 2011: HIV Causes AIDS

One of Rethinking AIDS’s greatest conceits is that it is a harmoniously functioning market place of ideas where a multiplicity of individual voices is allowed to be heard. President David Crowe decribes it as a forum where scientists can express their opinions and contrasts it with the scientific tyranny the Perth Group wants to impose on all dissidents, although by what means this would be remotely possible is not clear.  We maintain that the issue is deceptively framed and that ”harmonious multiplicity of individual voices” is a generous euphemism for cacophony of plagiarism, self-contradiction and substandard scholarship; for example when Prof. deHarven claims to have come up with a new original theory of HIV,  or when Prof. Bauer, Christin Fiala MD. and President Crowe argue in one context that HIV is a harmless passenger virus and in another that it has never been proven to exist, or when Prof. Duesberg claims that HIV has been satisfactorily isolated and sequenced, but claims that the many divergent HIV strains are an impossibility.

This generates general confusion, destroys credibility and creates a situation where the left hand doesn’t know what the right hand is doing.  For example, David Crowe has repeatedly been alerted by us, Fabio Franci MD and the Perth Group to the fact that Rethinking AIDS in appointing neo-duesbergian Prof. Marco Ruggiero to its Board is endorsing the claim that HIV causes AIDS, a claim which David Crowe has adopted as a rallying cry for the 2011 Rethinking AIDS convention in Washington. In a mail asking for convention donations, we read the following:

Dear Fellow AIDS Rethinkers:

With your help, a new phase of the struggle against the destructive hypothesis that HIV is the sole cause of AIDS is about to begin.

Dissent is not Denialism!

Why the addition of the word “sole”? It is Prof. Ruggiero’s formulation and it appeared on the Rethinking AIDS website at the time of his appointment to the Board of Directors. On that occasion Crowe wrote:

Dr. Ruggiero stated that in the past three years definitive evidence has accumulated demonstrating that HIV cannot be considered the sole cause of AIDS. For example, a ten year meta-analysis of anti-retroviral therapy published in the Lancet showed that, although the medicines decreased HIV levels, they did not decrease the rates of AIDS or death. Ruggiero concludes that the virus does not cause AIDS, but instead arises as a result of a lowered immune system, thus reversing the cause-effect relationship between HIV and AIDS.

Dr. Ruggiero referred to Nobel Prize winner Luc Montagnier who stated that someone with a healthy immune system can be exposed to HIV many times without being chronically infected. It is possible for someone infected with HIV to get rid of the infection by naturally building up their immune system, without the use of anti-viral medicines.

As we have seen, the uneasy tension between “cannot be considered the sole cause of AIDS” and “does not cause AIDS” had been resolved in favour of the first formulation by the time Crowe began sending out mails asking for donations. As Fabio Franchi noted in his reply to Crowe, that means the recipients of the mail were asked to donate to a convention premised on the belief that HIV can cause AIDS.  In spite of this, Crowe wrote a mail to the Perth Group saying:

I am also concerned about your distortions of the position of Rethinking AIDS which, on detailed scientific issues (such as the existence of HIV), often does not have a position but allows its members to think and speak for themselves. I don’t know where you got your assertion that “According to RA HIV is a cause of AIDS”. (…) I do not understand why you would deliberately distort what we have so clearly written and conclude that, “you accept that HIV is sexually transmitted and is a cause of AIDS”. First of all if “you” means David Crowe you know that this is a false representation of my beliefs. And if “you” means RA, while there are some who believe that HIV can be sexually transmitted, I don’t know of any who believe it is a cause of AIDS, which is by far the most important part of the belief. (Crowe to the Perth Group 17 August 2011)

If this is true, why specifically adopt the formulation “HIV is not the sole cause of AIDS”. Is it merely another awkward attempt at being politically sophisticated or does it represent a real shift?  Let us be clear:

1. Like Duesberg, Ruggiero thinks HIV exists as an exogenous virus, and like Duesberg this commits him in principle to the position that the HIV tests are reliable:

Any test, by definition, cannot be 100% accurate. Specificity and sensitivity often are inversely related; therefore un-specific diagnoses of HIV-positivity are likely to occur as with any other test. In general, however, once such problems have been resolved, I would say that in the presence of confirmed antibodies and detection of the so-called viral load (although often over-estimated), I would say that an encounter with the virus has occurred. (Ruggiero to Celia  Farber in “Over the Rainbow”)

2. Ruggiero thinks HIV is an effect rather than cause of immune deficiency (just as the Perth Group has argued for decades now), but it is an effect in Montagnier’s sense, an opportunist that is able to take hold when the immune system is already weakened. HIV, in other words, is one of the iconic AIDS pathogens like Pneumocystis jiroveci:

If we adhere to the statements of Prof. Montagnier, as I do, then the persistence of signs of HIV infection could simply be an indicator of immune system malfunction. In this interpretation, immune system malfunction is the cause and chronic HIV infection (along with other opportunistic infection) one of the effects, probably not the worst one. In other words, HIV infection could be the symptom of an existing immunodeficiency.  (Ruggiero to Celia Farber in “Over the Rainbow”)

Above, we called HIV an opportunistic pathogen, and the quotation shows why. Ruggiero speculates that HIV is “probably not the worst” effect of immune system malfunction, which implies that it is an undesirable effect. Ruggiero bases himself on Yamamoto and his GcMAF macrophage activator as well as Montagnier’s opportunisic HIV, and Yamamoto’s account of the mechanism by which HIV causes immuno-suppression is that it secretes nagalase which inhibits macrophage activation:

Serum Gc protein (known as vitamin D3-binding protein) is the precursor for the principal macrophage activating factor (MAF). The MAF precursor activity of serum Gc protein of HIV-infected patients was lost or reduced because Gc protein is deglycosylated by alpha-N-acetylgalactosaminidase (Nagalase) secreted from HIV-infected cells. Therefore, macrophages of HIV-infected patients having deglycosylated Gc protein cannot be activated, leading to immunosuppression. Since Nagalase is the intrinsic component of the envelope protein gp120, serum Nagalase activity is the sum of enzyme activities carried by both HIV virions and envelope proteins. These Nagalase carriers were already complexed with anti-HIV immunoglobulin G (IgG) but retained Nagalase activity that is required for infectivity.

HIV, intracellularly, as virions or as “free” gp120, is inherently immuno-suppressive, according to Ruggiero’s adopted position. In other words, it may not be the sole cause but it is certainly a contributing cause of  AIDS. And how do we know this is his final position and not another “Trojan horse”? Because we know that Ruggiero thinks HIV is real, that the HIV proteins are real, and that they can be reliably detected. This validates observations such as those made by Yamamoto. In fact, Ruggiero’s soon to be made commercially available GcMAF yoghurt is predicated on the validity of Yamamoto’s observations. Ruggiero’s new lay collaborator explains it admirably in this recent sales pitch, which went unchallenged on Prof. Bauer’s Hivskeptic blog – skeptic no more apparently:

Richard Karpinski said 2011/10/07 at 1:18 pm

DC asked “what is the benefit of taking substances that raise the CD4 count?” As you know, anti-retroviral drugs are themselves life threatening. Thus anything that keeps your CD4 counts high and reduces the pressure to start HAART “therapy” can be considered life preserving. Besides that, indications such as feeling better and having more energy are enough for me to desire to partake of MAF 3 14 on a regular basis, except when I’m pregnant. As a guy, I remain unlikely to become pregnant, but I am aware that fetuses (or possibly placentas) emit nagalase, which somehow prevents formation of GcMAF and thus prevents activation of macrophages, presumably to prevent them from attacking the fetus as cells which are not cells with the same chromosomes as those of the mother. Indeed, if gp120, thought of as an HIV viral coat protein, which also acts like nagalase and inhibits production of GcMAF, is a common component that triggers an HIV+ test result, then HIV+ IS itself an actual cause of partial suppression of the immune system. This would encourage me to take Ruggiero’s MAF 3 14 on general principles. But of course you should think that through on your own. IANAD, I am not a doctor.”

We remark in passing that unless it says on your cup of Ruggiero’s homemade, self-tested yoghurt that an increased level of CD4 cells is not considered a treatment benefit in itself but rather that it is the avoidance of HAART therapy that is the benefit, this could easily be fraud. But note also that a positive HIV test means you’re infected with a virus that can impair your immune system, a Human Immunodeficiency Virus as it were.  Karpinski’s logic is flawless; it is the logical extension of Duesberg’s position that HIV is real but harmless. To quote Eugene Semon:

If HIV exists, as Duesberg claims, then one has to test “harmless passenger” by considering cellular proteins within “purified virions” that may lead to autoimmune dysfunction. These cellular proteins (e.g. Hsp 70) are well known inflammatory agents, and the literature is chock full of papers on disorders when they’re over-expressed.

That is exactly what Ruggiero/Yamamoto has done; he has considered but one of the “harmless passenger virus” proteins and identified a mechanism by which “HIV” causes immune suppression. And this is not remarkable if one understands how the “HIVproteins” were discovered. They were chosen because they were found in abnormally high concentrations  or expressed and observed under abnormal conditions in already immuno-compromised individuals. That such proteins should have pathogenic effects under these circumstances is analogous to healthy cells becoming cancerous.

The consequence of all this is that Rethinking AIDS is now poised to market cures for HIV, literally, while its president David Crowe vehemently denies that he knows of any dissident who believes that HIV causes AIDS. Is Crowe deliberately lying? Probably not. It is more plausible that in the cacophony of plagiarism and self-contradiction that is Rethinking AIDS nobody is able to hear even their own words, much less understand what they mean.

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Why come to a Rethinking AIDS Conference or Didn’t Terry Michael get the Memo?

David Crowe’s latest discovery, Terry Michael, whom he brought in as co-host on his “How Positive are You” radio show has dissociated himself, or withdrawn his “participation and support” as he puts it, from Rethinking AIDS 2011 conference (As the second last line in the quotation shows, he is in fact dissociating from Rethinking AIDS altogether, and he is no longer co-hosting Crowe’s radio show.) The pattern is familiar, it happened last to Janine Roberts, if you assert yourself or stand on any kind of principle you will be labeled “uncooperative” by the Rethinking AIDS inner circle and your RA privileges will be revoked. Terry Michael:      

September 12, 2011

RA Board and other rethinkers:

Due to an irreconcilable difference with the other two organizers of RA2011, I am withdrawing my participation in, and my support for RA2011.

David Crowe and Siggi Duesberg seem to think the conference should be another effort at rethinkers talking to each other.  From the beginning, I promoted the mission of this conference as an outreach to the victims of HIV=AIDS–gay men, Africans and African Americans–who are not even represented on the RA Board. I urged that it be held in the epicenter of the HIV=AIDS myth, Washington, DC, with our large number of gay men and African Americans, and in the city that will be the venue seven months later for the International AIDS Society 2012 AIDS-fest conference of 15,000-20,000 cult members in Washington, DC.  I urged that the conference begin on World AIDS Day as a way to facilitate some kind of media attention for our effort.

I have spent countless hours in planning for the conference, beginning with visits to a half-dozen possible hotels ten months ago, including the one we eventually contracted with.  Though I have no personal wealth, I committed to $2000 in donations to RA, $1,250 of which I have donated, including paying the $150 registration fee.

The only thing I asked was to be able to do a two-hour special seminar for local people. This was after David and Siggi refused to even consider allowing local people to observe the conference without paying the steep registration fee.  The local attendees would be gay men and African Americans who have never heard of opposition to HIV=AIDS; just people who I would persuade to open their minds to hearing us.

I also recently urged that a student, young adult or low income special registration fee be offered, but again, Mr. Crowe and Ms. Duesberg just dismissed the idea.

And now, I understand that David is trashing me as uncooperative, trivializing my efforts.  It is correct that I am insisting on starting my seminar no earlier than 3:30 pm on World AIDS Day. It is an absolute fabrication that I EVER agreed to starting at 1 p.m.  I told David and Siggi a long time ago that my best guess is that the AIDS Industry here will be doing another free AIDS Day luncheon for members of the local Industry, and I wanted my seminar at the end of the day. To begin at 1 pm or 2 pm would mean local people would have to take off their entire afternoons from work.  I reluctantly agreed to 3 p.m. as a start time, and then Siggi and David arbitrarily demanded that I start at 2 pm.  I suggested that the conference start at 6:30 pm instead of 6 pm so I could start later. All of that was rejected by them–reflecting their lack of commitment to making this conference an outreach to the community of victims of HIV=AIDS.  And, RA Board members will recall the doom-and-gloom report that Ms. Duesberg gave in the last RA Board conference call, with an incredibly negative attitude toward the success of the conference.

I will continue to research and write about the HIV=AIDS myth, but I will do that independently from Rethinking AIDS.

I thank you all for your efforts at ending the psychological terrorism and the drug poisoning of the HIV=AIDS myth.

Regards,
–Terry Michael

Terry Michael confirms what we have shown again and again here on the Symposium and on TIG’s Rethinking AIDS page, that regardless of what altruistic motives the individual rethinker may have, the Rethinking AIDS entity and its annual conventions, like all things political, are nothing but vehicles for furthering personal ambition and sharing that feel-good vibe the privileged seem to crave.  This is the annual cleansing ritual where the plight of the excluded poor and African AZT babies is lamented by the self-satisfied in a cozy setting before an admiring,  like-minded audience on a full stomach - briefly before the after-party hobnobbing. Such is the nature of the political beast, but maybe you shouldn’t take our word for it, since we haven’t been there. Let the next Rethinking AIDS president Henry Bauer himself tell you what Terry Michael apparently hasn’t understood, just  how far such an event is removed from any concern other than elite recreation and self-congratulation, in his aptly titled blog post “Why come to a Rethinking AIDS Conference” :

Those of us who have belonged to professional organizations or academic associations or recreational groups featuring competitions like bridge or chess know how rewarding as well as enjoyable conferences can be —not so much because of the formal program or competition, but because of the opportunity to make new friends and to learn informally and person-to-person about all sorts of things that we didn’t even know existed to be learned about.
The first Rethinking AIDS Conference in Oakland in 2009  exemplified those delights. Over the years (>50!!) I’ve attended innumerable conferences of various sorts: academic, professional, or scholarly conferences in electrochemistry and in science & technology studies (STS); tournaments of bridge and chess; meetings of the National Association of Scholars, and of the Society for Scientific Exploration; International Science Conferences sponsored by the Unification Church; get-togethers of very specialized fan clubs interested in Loch Ness monsters or UFOs. No doubt others as well. A general conclusion, which is shared by all the people with whom I’ve talked about this, is that the most rewarding and enjoyable meetings are those that bring together people with the greatest diversity of backgrounds who happen nevertheless to share a passionate interest in the meeting’s particular focus. That’s exactly what I experienced at Rethinking AIDS 2009 in Oakland, and it’s why I wrote that somewhat over-the-top paean to the Conference  on my blog.
The Science and AIDS Conference in Vienna in 2010 was equally rewarding and enjoyable, yet very different in physical ambience; and most of the participants and observers had not been at Oakland, giving me the opportunity to make new friends. (etc. etc.)

There is scant room for community outreach of the sort Terry Michael proposes at the bridge tables of the conference’s star attractions, and just as was the case with the Perth Group, Terry Michael’s dissociation has been completely blacked out in all RA-controlled media allowing this to stand uncontested as the final reason why you should come to a Rethinking AIDS conference. So enjoy and…

 Bon apetit!

 CLAUS JENSEN

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The Potemkin Defence of Duesberg: Rescuing the Passenger Virus with the Missing Virus

According to the neo-Duesbergians in control of Rethinking AIDS, it’s strategically savvy to argue the scientifically flawed Passenger Virus theory because the important thing is to show that HIV doesn’t cause AIDS and the path of least resistance, so the argument goes, is the least radical counter to the orthodox HIV > AIDS theory. In particular David Crowe and Henry Bauer have argued that Judge Sulan’s ruling in the Parenzee case was proof that the Missing Virus approach is extreme and unnecessary. The argument is dishonest and adds insult to injury because it was Crowe himself who managed to change defence lawyer Kevin Borick’s strategy to conform with the Passenger Virus theory that HIV is difficult (but not impossible) to transmit sexually but harmless in any event. In fact, this change of strategy itself as well as its substance were soundly defeated in the Parenzee case.

But the neo-Duesbergian strategy has been tested even more directly outside the courtroom. Duesberg’s et al  Passenger Virus theory, set forth in Medical Hypotheses was critically examined both by us and by the orthodox HIV professionals. In both cases the neo-Duesbergians responded with rebuttals of the criticism, thus providing a test case for how well their strategy holds up under pressure.  It turned out that in both cases, the neo-Duesbergians almost immediately had to fall back on the Missing Virus science of the Perth Group to defend Duesberg’s passenger virus.

In our analysis of Duesberg et al, we concluded that Duesberg’s acceptance of the Orthodoxy’s claim that HIV has been isolated, and consequently the validity, at least in principle, of the HIV tests and HIV epidemiology, creates many of the same inconsistencies and paradoxes that it does for the mainstream HIV>AIDS theory. Duesberg et al notably used inflated antenatal statistics on South African HIV prevalence peaking at 25-30% in support of  the Passenger Virus theory, while at the same time dismissing similarly generated statistics on AIDS mortality.  For AIDS mortality they claimed instead that a count of the actual death certificates rather than estimates based on various models is an accurate reflection of conditions on the ground, and in this way, by accepting HIV prevalence estimates but rejecting the AIDS mortality estimates, they were able to create an impressive disconnect between HIV and AIDS, which is the core epidemiological argument for the Passenger Virus theory.

Duesberg et al. have since repeatedly affirmed that in their opinion these numbers, especially AIDS mortality, should be taken at face value, so let’s do just that: An annual mortality of 10-15,000 among HIV positives corresponds to about 2.5% of total annual mortality in South Africa. This means that either South Africans have an uncanny ability to differentiate between an HIV-related and a non-HIVrelated AIDS indicator disease in HIV positive people or the 25-30% of the population who are HIV positive only account for 2.5% of the total mortality plus those deaths that are easily classified as not HIV-related and thus presumably would not be counted as AIDS deaths (mainly in the “unnatural causes” category). But the latter are unlikely to make up for the missing  25% of total mortality, since AIDS has been carefully defined to include almost all common natural causes of death. According to Duesberg et al., then, HIV is a marker for excellent health and unusual longevity in South Africa. It’s hard to judge who is fonder of HIV, the followers of the Pathogenic Virus theory or the followers of the Passenger Virus theory.

Duesberg responded to the critique by distributing and endorsing, a defence of his MH paper written by Joyce Arthur assisted by David Crowe. In order to save Duesberg et al, the author(s) introduced the remarkable claim that the paper was simply “showing the expected (HIV) prevalence rates based on the orthodox data”, and that we should not be fooled into thinking that those rates are accurate or that the authors believe they are accurate. But the HIV prevalence rates cited by Duesberg et al were in fact not based on the generally accepted orthodox data, which put them considerably lower, but cherry-picked in order to 1) show the largest possible disconnect between HIV prevalence and AIDS mortality 2) show positive evidence of the Passenger Virus theory. If the authors don’t believe in the figures they use to advance their own theories it amounts to intellectual fraud. Remarkably co-author Henry Bauer all but admitted as much when confronted with the issue:

1. My apologies to many people for giving apparent comfort to Snout et al. in the article by Duesberg et al. which was rejected by at least 2 journals before making it into “Medical Hypotheses”. 2. Explanation — but I’m not asking to be excused. I should have been more scrupulous in checking successive drafts circulated among several authors. Perhaps I should have insisted on a footnote or the like pointing out that I neither support nor reject the “passenger virus” hypothesis while agreeing 100% with the main point of the article. Chigwedere et al. relied on spurious computer-generated estimates that differ from actual South Africa Statistics data by a factor of about 25. Perhaps I was wrong in thinking that the “passenger virus” issue isn’t important, just because it isn’t important TO ME. ( Public mail 26 June 2009)

If the Passenger Virus issue isn’t important to Bauer, one wonders why it figures so prominently in a paper he has co-authored for publication. It is debatable what is worst, intellectual dishonesty compounded by the dishonesty of Bauer’s mea culpa, or the indifference and sloppiness he confesses to in order to cover up his dishonesty. The Passenger Virus theory is the counter theory set up as an alternative to Chigwedere’s at al accusation, it takes up one third of the paper, and here one of the authors plainly admits when challenged that he doesn’t believe in it. This means that not only do the authors not believe in the statistics they use to argue their conclusions, they don’t even believe in the theories they are arguing for. Why, one asks, did the authors not argue for their real beliefs instead of publishing an intellectual fraud? The presumed answer is that it is consistent with the neo-Duesbergian strategy of taking the least radical path at all costs.

When  Chigwedere et al published their own rebuttal to Duesberg et al, David Crowe went solo on Rethinking AIDS court stenographer Celia Farber’s now defunct thetruthbarrier.com. Crowe attempted to go through Chigwedere’s points one by one but didn’t get very far, possibly because he never understood that Chigwedere’s argument hinged on Sir Bradford-Hill’s guidelines for assessing causality and so had no real notion of where he was going. On those points that have to do with HIV, Crowe argued as follows:

HIV has never been purified (…) The (HIV molecular) clone (allegedly infecting a lab worker) might have been pure, but where did it come from? Not from pure virus because there has never been any. (…) A naïve observer would assume that it means purification, based on the latin root “isola,” meaning “island.” But no, isolation now means what a virologist wants it to mean, no more, no less (apologies to Lewis Carroll). Isolation can mean the detection of a particular protein, p24, that is found widely in HIV-negative people and found only about half the time in HIV-positive people. Or it can be the indirect detection of reverse transcription, a process that is not unique to viruses, let alone HIV. Or it can mean cell death, the formation of giant cells (Synctitia (sic))  in culture that are never found in even the sickest AIDS patient. But one thing it never means is purification of the virus, separation of the virus from all other organic materials.

Needless to say, this is the Missing Virus argument being used repeatedly in Duesberg’s defence, by the same David Crowe who based his interference in the Parenzee case as well as the general strategy of the Rethinking AIDS organisation on the conviction that this approach is a “strategic blunder”. If we go back to Joyce Arthur, her “defence” of Duesberg has two legs. One is the “Duesberg et al don’t believe in the sources they’re using nor in the theories they’re advancing” argument we examined above. Her second argument is that the HIV tests are faulty and her reference is a blog post by none other than Henry Bauer, arguing that:

‘the hypothesized “HIV” – virions of which have never been isolated directly from “HIV positive” people’ is not what the HIV tests detect under any circumstances.

Naturally, David Crowe, Joyce Arthur and Henry Bauer all contrive to use the Perth Group’s Missing Virus science in their own and Duesberg’s defence without ever mentioning who originated it, but the fact remains that the  leading neo-Duesbergians, including those who hypocritically feign indifference to the Missing Virus issue can’t get a defence of Duesberg off the ground without making it the cornerstone of their argument.

CLAUS JENSEN

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