HIV/AIDS Skepticism

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

Archive for July, 2016

HIV infectivity: high, low, or non-existent?

Posted by Henry Bauer on 2016/07/31

Analysis of essentially all published results of HIV tests in the USA reveals properties unlike those of an infectious agent (The Origin, Persistence and Failings of HIV/AIDS Theory, McFarland 2007).  In every social sector, the same regularities are seen: rates of testing positive vary by US official “racial” and ethnic classification (black >> native American > Caucasian > Asian); rates of testing positive decrease drastically from birth into the teens and increase from the late teens into middle age and then decline again; in early teens, females are more likely to be HIV+ than are males but by the 20s that is reversed (see references cited in section 3.3.5 in The Case against HIV).

In cloned HIV virions, only between 1 in 10,000 and 1 in 10 million were infectious (Layne et al., “Factors underlying spontaneous inactivation and susceptibility to neutralization of human immunodeficiency virus”, Virology, 189 (1992) 695-714).

The instructions that come with HIV test kits warn that a positive test is not proof of infection.

Innumerable conditions produce HIV+ results (see references cited in section 3.2 in The Case against HIV), so all claims to have measured infectivity or transmission are at best dubious and at worst — or more accurately — meaningless. There is no valid published evidence of transmission or infectivity (see references cited in section 3.3 in The Case against HIV). The Office of Medical and Scientific Justice successfully defended more than 50 individuals charged with transmitting HIV because the prosecution could not prove HIV to be transmissible.

Researching phantoms

It can take a long time before researchers realize that they have been on a wild-goose chase, pursuing phantoms (“Phantom phantoms”, pp. 110-116 in Fatal Attractions: The Troubles with Science, Paraview Press 2001); even “an unknown phenomenon [that] towered 6 standard deviations above the mundane background of known physics — enough to satisfy a 99.9999% confidence level that it wasn’t a fluke” and that had been reported in more than a dozen experiments turned out to be non-existent.

Given that HIV/AIDS theory is wrong (The Case against HIV), observations and experiments and clinical trials will continually throw up what seem to be conundrums, which serve as the basis for yet more research. To date, mainstream HIV/AIDS researchers have failed to recognize the accumulation of conundrums and absurdities  as being in reality the hard evidence that HIV/AIDS theory is simply wrong: HIV is not infectious, and “HIV” doesn’t cause AIDS.

Mainstream science sticks to theories that had once been accepted by ignoring anomalies, conundrums, absurdities for as long as possible (Thomas S. Kuhn, The Structure of Scientific Revolutions, University of Chicago Press 1970 [2nd ed., enlarged; 1st ed. was 1962]). Things that don’t fit an existing theory are accommodated by ad hoc adjustments (Imre Lakatos, “History of science and its rational reconstruction”, pp. 1-40 in Method and Appraisal in the Physical Sciences, ed. Colin Howson, Cambridge University Press 1976), just as Ptolemy long maintained belief in the circular perfection of heavenly motions by adding epicycles upon epicycles, wheels within wheels, to avoid acknowledging that the movements are not really circular after all.

So too HIV/AIDS researchers create new hypotheses to bolster their belief whenever they seem unable to explain what they observe. Since all the data point to HIV not being infective, or being apparently infective to so low a degree as to be incapable of producing an epidemic, auxiliary hypotheses were suggested which have become accepted as shibboleths:

  1. The epidemic in Africa is said to have come about because of an incredible rate of promiscuity. Sexually active South Africans (black South Africans, that is) are postulated to have an average of 10 sexual partners at any give time and to change them about annually (pp. 63-65 in James Chin, The AIDS Pandemic, Radcliffe 2007).
  2. Soon after initial infection, there is an “acute phase” where large amounts of HIV are present, and intercourse during that phase makes transmission much more likely: infectivity is very high during these short periods, so overall measurements of transmissibility are deceiving.

The first suggestion is absurd, since such behavior would be so visibly evident that it could not be overlooked; yet it is not observed.

The second suggestion has been undermined by a careful re-analysis of the single study on which it had been based: the “excess hazard-months attributable to the acute phase of infection” is about 5.3, not the previously estimated 31-to-141 (Bellan et al., “Reassessment of HIV-1 acute phase infectivity: accounting for heterogeneity and study design with simulated cohorts”, PLoS Medicine, 12(3):  e1001801).

HIV/AIDS research is chasing red herrings, phantoms, in a decades-long wild-goose change that has been enormously expensive in lives and in dollars. But the interests vested in this state of affairs — drug-company profits, research careers, administrative careers, honors and awards — are so widespread and powerful that the actual evidence is given little or no chance of speaking for itself. Try to imagine what it would take for Anthony Fauci to shed cognitive dissonance and admit that he has been so disastrously wrong.


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