[In June 2012 Martin Barnes held an AIDS dissident conference in his village Vers Pont du Gard in the south of France. The first item on his agenda was 'The HIV puzzle -- what is being measured?' The Perth Group address this and the legal strategy implications arising from it. AB]

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.

  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:  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 Richards’ affidavit and David Steele’s interview with Celia Farber.

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 ).  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.


July 31st 2012

The Perth Group

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