HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Transmission of HIV cannot be proved

Posted by Henry Bauer on 2011/08/07

“Genetic analysis has shown . . .” makes the claim that something has been proven scientifically, which is commonly taken to mean beyond any doubt.
I’ve long wondered how such claims could be made with respect to HIV, since HIV is also said to mutate at such an astounding rate that
“no two virus isolates are identical….  Within a single … host, HIV-1 population represents a complex mixture, or swarm, of mutant virus variants … [whose] prevalence … is changing … on almost a daily basis (intrahost evolution)”
— Lukashov, Goudsmit, & Paxton, “The genetic diversity of HIV-1 and its implications for vaccine development”, ch. 3, pp. 93-120 in AIDS Vaccine Research, ed. Wong-Staal & Gallo, Marcel Dekker  2002.
Furthermore, one should not imagine that “genetic analysis” means that genomes are being compared, that whole DNA or RNA chains are being compared. Rather, the researchers decide to focus on some short segment of the presumed HIV genome and compare that short segment in the various samples.

Reliance on HIV genetic analysis has become increasingly common in criminal cases when an individual is charged with transmitting HIV. Earlier this year, Lancet Infectious Diseases (Abecasis et al., “Science in court: the myth of HIV fingerprinting”, 11: 78-9) published a clear exposition of the reasons why HIV genetic analysis cannot provide proof of transmission:
“the risk  of incorrect conviction is substantial because of a flawed  view  of  the  science  behind  forensic  phylogenetics.  A  scientific discussion of  HIV  fingerprinting  in  cases of  HIV  transmission is therefore urgent. . . . By  calling  such  investigations  HIV  fingerprinting,  scientists  raise  unrealistic  expectations . . . . Unlike   for   DNA   fingerprinting,  where  a  likelihood  can  be  calculated for  a  full  match between the evidential DNA and the suspect DNA, there  is never a full match between the RNA or the DNA of HIV  in two samples, even within an individual. HIV is constantly evolving *”
* Shankarappa et al., “Consistent viral evolutionary  changes associated with the progression of human immunodeficiency  virus type 1 infection”, Journal of Virology 73 (1999) 10489-502

This means that one can calculate only probabilities, in the first instance the probability that two samples come from the same hypothesized chain of transmission. Even when that probability is high, however, the data cannot distinguish between direct and indirect transmission in that chain: in other words, the supposed victim of transmission (V) might have been infected by someone other than the suspect (S) because S might have infected A, B, C . . ., any one of whom might have infected V.
Beyond that, a high probability that two samples come from the same chain of transmission says nothing about the direction of transmission: it might even have been V who infected S rather than the opposite.
Above all, it should be recognized that all evidence from genetic analysis is no more than circumstantial. It should not be confused with proof.
The point made by Abecasis et al. was seconded by Leitner et al. (Nature 473 [2011] 284; the correction published 6/7 July does not pertain to the following point):
“Scientists must explain to  courts that phylogenetic analysis  cannot ‘prove’ any particular  hypothesis . . . . results may be compatible with  several hypotheses, or support  one over another. . . . Although the direction  of viral transmission can  sometimes be supported, it does  not prove direct transmission.”
The AIDS Beacon website (“Independent, up-to-date news and information about HIV and AIDS”) interviewed authors of the Lancet article who emphasized, “Phylogenetics can prove that people cannot have infected each other, but it can never prove that people infected each other.”
Guidelines are being drafted for how researchers should give testimony about HIV phylogenetic analysis, in view of the universal agreement that it should never be described as “fingerprinting” and that courts should understand that

phylogenetics alone can never prove transmission:
 it can never prove any alleged transmission
occurred between two specific individuals.

I’ve not yet seen a discussion of how this point applies to research that attempts to trace where HIV first entered human beings; or more important, how this point applies to research on measuring supposed rates of transmission, and on studies of attempts to prevent transmission.
As it happens, Cohen et al. recently published “Prevention of HIV-1 infection with early  antiretroviral therapy” (New England Journal of Medicine, 10.1056/NEJMoa1105243, 18 July 2011) in which they claim that “The early initiation of antiretroviral therapy reduced rates of sexual transmission of  HIV-1”.
The studied population comprised 1763 HIV-1 discordant couples in 5 African countries and in Brazil, India, Thailand, and the USA. Early antiretroviral treatment appeared to result in transmission at a rate of 0.3 per 100 person-years, whereas the untreated population showed a rate of 1.2 per 100 person-years. The total number of actual apparent transmissions was 39:
“Through viral genetic analysis, 28 transmissions  were linked to the HIV-1–infected participant”.
But genetic analysis cannot prove such linkage!
Note too that 11 of the 39 apparent transmissions were not even claimed to be direct transmission. How did they occur?
Perhaps the same sort of process that produced these unlinked seroconversions might also have caused the 28 apparently linked transmissions as well?
Furthermore, 23 of the 28 purportedly linked transmissions were at African sites. It is mainstream dogma that the prevalence of HIV in Africa bespeaks a very high level of multiple concurrent sexual relationships. Since genetic analysis cannot prove any given case of transmission, it seems unwarranted to assume that those 23 apparent transmissions in particular can be taken as proven direct transmission within the discordant couple.
There are a number of other reasons as well for questioning the validity of conclusions from this study, for example the wide variety of antiretroviral drugs used: “Study drugs included a combination of lamivudine  and zidovudine (Combivir), efavirenz, atazanavir,  nevirapine, tenofovir, lamivudine, zidovudine, didanosine, stavudine, a combination of lopinavir  and ritonavir (Kaletra and Aluvia), ritonavir, and a  combination of emtricitabine and tenofovir (Truvada). A prespecified combination of these drugs  was provided to participants at monthly or quarterly visits. Sites could also use locally supplied,  FDA-approved drugs if they could be purchased  with nonstudy funds. For participants with virologic failure, specified second-line treatment regimens were provided”.
Even on the study’s own terms, surely one would need to consider the possibility that only one or some of these were effective, instead of lumping them all together as “early versus delayed therapy”?
Beyond that, it seems rather unlikely that precisely the same protocol and level of supervision could have been in effect in all the different study sites in the different countries, and with investigators that number at least the named 35 co-authors.

The chief point, however, is this. Experts in phylogenetic analysis are unanimous that this procedure cannot prove any given case of transmission. Cohen et al. rely on it precisely for such proof, and therefore their conclusions cannot be accepted as valid. Less politely, one might say that this peer-reviewed paper is BS.

*                    *                    *                    *                    *                    *

Most studies of claimed transmission have relied  only on “HIV” tests. Those are even less to be believed, of course, than the genetic analyses, given the high rate of seroconversion for reasons having nothing to do with “HIV infection”. Just as with genetic analysis, though, an absence of matching tests can demonstrate a lack of transmission, as in the notorious Padian study.

15 Responses to “Transmission of HIV cannot be proved”

  1. Martin said

    Hi Dr. Bauer, several things come to mind with this excellent post. Since there’s nothing in the literature demonstrating viral isolation of HIV from any human being. And this so-called mutation scam that establishment scientists keep insisting upon. How is it these scientists can claim this purported retrovirus can be mutating when they’ve (1) never isolated one and (2) never demonstrated how it (HIV) makes people sick. Well, it looks like their mendacity may be finally catching up with them.

  2. Guy said

    Dr. Bauer,

    Can we take the rate of transmission of 1.2 per 100 person years to provide further evidence that HIV is not sexually transmitted?
    Do they check out HIV seronegative people to see if they have what are considered to be HIV viruses? IE give the blood to a scientist and not tell him the serostatus of the donor and ask to look for HIV.
    Did they retest the seropositives to see if any reverted to negative serostatus?
    If they relied on HIV tests to determine seropositivity, could the seeming better results for the ARV takers owe to immunosuppression? In other words, the group taking the medicines and the ones not might have the same proteins in their veins, but the ones taking the medicines are not producing the anti-bodes as effectively.
    I believe it is Dr. Roberto Giraldo who argues that the proteins that cause the seropositivity are generated by cell destruction caused by oxidative stress. Could we be studying cell debris and considering it to be viral?

    • Henry Bauer said

      Guy:
      with the proviso that it is APPARENT transmission at such a low rate. With real STDs like syphilis or gonorrhea, transmission probabilities are appreciable percentages (20% – 50% or more) PER ACT OF INTERCOURSE. At only 1 act per week, 20% translates to 10 per 100 person-years….
      CORRECTION (see Rchard Karpinski comment):
      At only 1 act per week, 20% translates to 1000 per 100 person-years. Apparent transmission of “HIV” is many hundreds of times less than that of real venereal (sexually transmitted) diseases.

      • ale said

        Hi D. Bauer. What do you think about a theory that says that aids is caused by a mycoplasma weaponized with components of another new virus (real aids virus -not hiv-) ? i have seen it on questioningaids site, written by a supposed virologist.. thank you.¡

      • Henry Bauer said

        ale:
        Sorry, I don’t know about this weaponizing. I do know that Montagnier long ago, and also Lo, believed that what was killing T-cells in their “HIV” “isolates” and cultures was mycoplasma, not HIV — because tetracycline antibiotic, which does not kill virus, blocked the killing of T-cells.

      • “At only 1 act per week, 20% translates to 10 per 100 person-years….”

        At 20% per act, and 50 acts per year, I would calculate 10 per person year or 1000 per 100 person years. That’s a very different result. Which of us has miscalculated?

      • Henry Bauer said

        Richard Karpinski:
        I accept your rhetorical question :-)==
        Many thanks for the correction.
        The supposed transmissibility of “HIV” is many hundreds of times less than that of known STDs.

  3. BSdetector said

    An email conversation I had with the esteemed Nick Bennett involved this post. I asked Dr. Nick if there is a “Swarm” of HIV supposedly fluttering about the body, then why has the probe used for “HIV Viral Load” not changed in over 10 years. He responded that although “HIV” mutates at a great rate, the probe hybridizes with a part of HIV that does not mutate. Then I asked him the nature of the mutation process, what exactly causes the mutations (which I already knew). The mutations are caused by the inefficiency of the reverse transcription enzyme. It makes many more mistakes than DNA polymerase. So, if the mutations are caused by reverse transcriptase, then each base would have the same potential for mutating as any other? Yes. So, based on this theory, there is no part of the HIV genome which would remain free of mutations, because the inefficient reverse transciptase transcribes the entire HIV genome from RNA to DNA. If there was in fact a swarm of constantly mutating HIV in the body, no PCR probe could ever be constructed that would find any more than a small number of the total “swarm”. At this point he stopped responding to my emails…go figure.

    • TD said

      It’s not that mutations don’t occur, mutations in certain regions, particularly Gag, lead to non-viable genomes. Therefore those parts of the genome inevitably remain relatively conserved. Very straightforward. As a loose analogy, a human being can tolerate lots of external variability but our internal organs are very conserved, and mutations that disrupt their function don’t persist the way mutations that alter eye and hair color do, for obvious reasons.

      • Henry Bauer said

        TD:
        Please expand on that.
        What do you mean by a “non-viable genome”? The genome disrupts? So then the bits of it are still there. And PCR only picks up bits, not whole genomes.
        Please also explain how the “HIV genome” was first characterized, since no pure bona fide virions of “HIV” have ever been isolated. If such virions were available, then they could be used to validate gold-standard HIV tests, and there are no such tests — see Stanley H. Weiss & Elliot P. Cowan, “Laboratory detection of human retroviral infection”, chapter 8 in Gary P. Wormser (ed.). AIDS and Other Manifestations of HIV Infection. London etc.: Academic Press; 2004 (4th ed.).

  4. Francis said

    I’d think that the fact that no two HIV samples are ever the same gives more weight to an endogenous retrovirus being generated in the presence of an already present disease state. The alleged mutation rate is more likely the result of differences in individuals DNA expressing this retrovirus than in the “Swarm” theory in vogue. Clades are also more likely the result of general similarities in populations DNA in distinct geographic areas rather than a propensity for the virus to prefer not travelling.
    There are so many inconsistencies and outright lies in HIV/AIDS “Science” that the only mysterious thing about this virus is that it is still believed to exist as an exogenous pathogenic viral entity by the orthodoxy.

  5. KC Blair said

    Hello, Henry and readers. Thank you for what you do, Henry.

    I used to follow the HIV-AIDS hypothesis science until I learned there is no correlation between HIV and AIDS. I began to realize HIV-AIDS is an ongoing story with no facts or validity and definitely not based on science. This saddens me because people I have known, thinking they had AIDS, died from something else — the toxic medical treatment for something they did not have?

    Finding the HIV-AIDS relationship an illusion, led me to a higher level of skepticism. I began to study the relationship between modern medicine and our overall health. I presented a paper of my findings, MODERN MEDICINE: AN ILLUSION, http://www.goodsamiam.com/SSE-2006-Paper.pdf to the Society for Scientific Exploration. http://www.scientificexploration.org/

    In summary, changes in our exposure to modern medicine are inversely correlated with changes in our overall health. (Changes in exposure lead changes in health.) Furthermore, it looks like 50% of the people dying each year are dying from to the iatrogenic effect, i.e. the unintended consequences from exposure to allopathic medicine. Henry once told me he could find no published theory of allopathic medicine. I couldn’t either and now I think I know why.

    Included in the paper and my website, http://www.GoodSamIAm.com, is a different but validated view and strategy for living a healthier, happier, and longer life based on our findings of the placebo and its compassion effect, over which we have control.

    I wish you well.

    KC Blair

    P.S.: If you read my paper the Appendices are also worth reading.

  6. Maurits said

    Dr. Bauer,

    Science Magazine has selected the Cohen et al. publication to be the “Breakthough of the Year 2011” :
    http://www.sciencemag.org/site/special/btoy2011/
    They obviously haven’t read your blog!

    • Henry Bauer said

      Maurits:
      Yes. SCIENCE and NATURE would be much more reliable if they read and paid attention to my blog 😉

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