HIV/AIDS Skepticism

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

Posts Tagged ‘HIV is not infectious’

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.


Posted in clinical trials, experts, HIV absurdities, HIV and race, HIV does not cause AIDS, HIV tests, HIV transmission, HIV varies with age, HIV/AIDS numbers, Legal aspects, M/F ratios | Tagged: , | 18 Comments »

HIV, AIDS, and age: HIV/AIDS theory is wrong

Posted by Henry Bauer on 2009/01/23

People between 35 and 45 years of age are most affected in everything to do with HIV/AIDS: testing “HIV-positive”, living with HIV/AIDS, being diagnosed with AIDS, dying from “HIV disease”. That should astonish anyone who thinks about it. In and of itself, this indicts HIV/AIDS theory as wrong.

When first named in the early 1980s, AIDS was diagnosed in people (largely men) whose average age was in the mid-30s (A). That already throws into serious doubt the notion that AIDS is brought about by a sexually transmitted agent, because it’s teenagers and people in their early twenties who are most prone to incur sexually transmitted diseases (STDs) or infections (STIs) (B).

At that time, the early 1980s, death was believed to follow within a few years of “infection” — recall, for example, that the airline steward “Patient Zero” had been held responsible for the spread of AIDS because he had been promiscuously sexually active, only months earlier, in places where the illness first became prominent (C). But even if one projects into the past the current much longer estimate of about 10 years for the “latent period” between “infection” and illness, one is still forced to infer that the maximum risk of getting “infected” with “HIV” had been for individuals in their mid-20s, which remains significantly later than is the general experience with STDs.

There is direct evidence, however, contradicting any speculation that infection by “HIV” is most likely among people as young as the mid-20s. The results of “HIV” tests at public testing sites (roughly 2 million tests annually) have been reported, by age, from 1995 to 2004 (D). Calculated from those data, the median age of those testing positive increased gradually from 34 in 1995 to 37.5  in 2004; even extrapolating that trend back to 1980 brings the median age down no lower than 29. Not that those tested were for some reason concentrated in the mid-30s age group: the median age of those tested was 27.8 in 1995 and 28.7 in 2004. The mid-30s age of those testing “HIV-positive” has to do in some manner with the “HIV” tests, it is not an artefact of the ages of those who were tested.

So not just AIDS diagnoses and “HIV disease” deaths are most encountered in people aged between the mid-30s and mid-40s, so are positive “HIV” tests — all occur at least a decade later than the usual age of maximum risk for an STD.

Of course, the age at which the first positive “HIV”-test is reported is not the age at which “infection” or seroconversion occurred. However, the first report from the Centers for Disease Control and Prevention in which time of new “infection” is estimated by a recently developed scheme yielded 35.1 as the median age of “first infection” in 2006 (E), once more: a good decade-and-a-half older than where STDs usually strike with greatest frequency. Comparing that 35.1 with the 37.5  for first positive test in 2004 suggests a difference of no more than 2 or 3 years on average between “new infection” and first positive test, which is entirely plausible, since individuals who suspect themselves to be at risk are likely to seek testing rather frequently, especially after risky encounters. That first positive tests come at a median age in the mid-30s or somewhat later is not compatible with the hypothesis that a positive “HIV”-test signifies a sexually transmitted infection.

(I had become convinced that “HIV” is not an infection upon seeing how regularly the rate of testing “HIV-positive” varies with age, sex, and race. For that reason, I’ve remained interested in those variables. So I note here that the median age for testing “HIV-positive” in this population (D) was 1.6 years greater for white men than for white women, and 1.8 years greater for black men than black women; for black men it was 1.1 years greater than for white men, and for black women 0.9 years greater than for white women —  perhaps ±20% in each case.)

In 1995, the median age for new diagnoses of AIDS was 37.3, in 2004 it was 40.7 (E). Thus the average interval between greatest probability of a first positive “HIV” test and of a new AIDS diagnosis was only 3.3 years in 1995 and 3.8 years in 2004, about one third of the putative “latent period”. Even adding the possible 2 to 3 years between “new infection” and first positive test leaves the interval at a half or two thirds of the postulated latent period. Even if one over-simplifies drastically, and suggests that “new infections” of those first testing positive in 1995 occurred at average ages of 31-32 to produce most of the deaths in 2004 at average age 45, that offers no hint of any prolongation of the purported 10-year latent period during this period in which HAART is supposed to have provided life-saving benefits extending life spans by anywhere from 7 years initially to several decades now.

It’s surely a truly strange situation. The first AIDS cases, in the early 1980s, were among people in their mid-30s. Two decades later, it’s still people in their mid-30s who are most likely to test positive for the purported agent that supposedly produces AIDS on average roughly a decade after “infection” — with the added oddity that “AIDS” seems to strike within significantly less than a decade after “infection”, despite firm claims that treatment successfully staves off illness. On the face of it, this is so incompatible with HIV/AIDS theory as to effectively falsify it.

But that’s far from all. Not only positive “HIV” tests and new diagnoses of “AIDS” peak among people in their mid-30s to mid-40s, so do deaths ascribed to HIV/AIDS. The median age for those deaths was 35.8 in 1982, increasing gradually to 45 in 2004 [Table 2 in “HAART saves lives — but doesn’t prolong them!?”, 17 September 2008].

Here are all those numbers again:


A more complete argument to the same conclusion considers not just median ages but the whole age distributions [“HIV Disease” is not an illness, 19 March 2008; “Incongruous age distributions of HIV infections and deaths from HIV disease: Where is the latent period between HIV infection and AIDS?”, Journal of American Physicians & Surgeons 13 [#3, Fall 2008] 77-81);  How “AIDS Deaths” and “HIV Infections” Vary with Age — and WHY, 15 September 2008]. The age distribution of first positive test must be broader than that for initial “infection”, because those “infected” at a given time will seek testing over a range of time. For the same reason, the age distribution for illness must be broader again, and that for deaths broader still. The actual data, however, show the age distribution of deaths to be, if anything, narrower than the others [No HIV “latent period”: dotting i’s and crossing t’s, 21 September 2008]:

2hivdeathsmidline (widths were estimated at half peak height,
not where the horizontal lines are in the figure)

Moreover, all the age distributions have shifted very little over the years, as illustrated by the very gradual shift in median ages [and see Figures 2a,b in “No HIV ‘latent period’: dotting i’s and crossing t’s”, 21 September 2008.]. The age distribution of deaths has remained, throughout, virtually superposable on the age distributions of first positive tests, and of diagnoses of illness, — which thereby demonstrates both lack of any significant “latent period” and lack of any significant life-extension from antiretroviral drugs.

Beyond all that: the age distribution of deaths is, in and of itself, independently of the argument above, a strike against HIV/AIDS theory. In all illnesses and diseases, among those who are stricken it is young-to-middle-aged adults who survive better than do older adults or very young children [see, for example, for influenza, Figure I in “Living with HIV; Dying from What?”, 10 December 2008]. With “HIV/AIDS”, however, that is not at all the case: the probability of dying from “HIV disease” among those who are “infected” does not increase rapidly with increasing age [see Table II  in the same post as Figure I].

Nothing about age and HIV/AIDS makes any sense. The numbers simply don’t add up — or, rather, they add up to a resounding disproof, a series of disproofs, of the misguided hypothesis that “HIV” caused “AIDS”.


A few sources for this are cited at pp. 87-88 in The Origin, Persistence and Failings of HIV/AIDS Theory. The annual “Health, United States” reports show the median age for new diagnoses of AIDS to have increased gradually from 35.1 in 1982, reaching 41 by 2005  [Table 2 in HAART saves lives — but doesn’t prolong them!?, 17 September 2008].

For example:
“Sexually Transmitted Disease Surveillance, 2007
STDs in Adolescents and Young Adults
Compared to older adults, sexually-active adolescents 15 to 19 years of age and young adults 20 to 24 years of age are at higher risk for acquiring STDs for a combination of behavioral, biological, and cultural reasons. For some STDs, for example, Chlamydia trachomatis, adolescent women may have a physiologically increased susceptibility to infection due to increased cervical ectopy. The higher prevalence of STDs among adolescents also reflects multiple barriers to accessing quality STD prevention services, including lack of insurance or other ability to pay, lack of transportation, discomfort with facilities and services designed for adults, and concerns about confidentiality. Recent estimates suggest that while representing 25% of the ever sexually active population, 15 to 24 year-olds acquire nearly half of all new STDs.”

“Report: Student STD risk hits 50%
North Carolina researchers found nearly half of all STD cases in the United States occur in 15 to 24 year olds” by Lisa Catto

“Recent surveys in several countries have shown that the prevalence of STDs is higher among women under 20. In general, adolescent males and females, are at greater risk for contracting STDs”, citing Brabin et al., Lancet, 345 [1995] 300-4; Duncan et al., Lancet 335 [1990] 338-40; Duncan et al., Central Africa Journal of Medicine 40 [1994] 234-44; Lema et al., East African Medical Journal 71 [1994] 122-8.

“Sexually experienced adolescents less than 19 years of age are at greater risk for the acquisition of sexually transmitted diseases (STDs) and typically have higher STD rates than other age-specific groups. Nationally, this population accounted for about a quarter of all reportable STDs”; project on HIV/STD Risk Reduction for African American Adolescents, Kaye Sly (Principal Investigator) Jackson State University, Mississippi

(C) Randy Shilts, And the band played on: politics, people, and the AIDS epidemic, St. Martin’s, 1987.

(D) Centers for Disease Control and Prevention: HIV counseling and testing in publicly funded sites: 1995 summary report (September 1997);  1996 annual report (May 1998); annual report 1997 and 1998 (2001); HIV counseling and testing at CDC-supported sites —United States, 1999–2004 (2006);

(E) “Subpopulation Estimates from the HIV Incidence Surveillance System — United States, 2006”, MMWR 57 #36 [12 September 2008] 985-9, see Table E at p. 987. Lack of data for ages ≤13 is unlikely to add seriously to the considerable uncertainties associated with how new infections are estimated; for instance, at public testing sites, 1999-2004 (see citation in reference (D)), HIV-positives under 13 made up only about 0.1% of white HIV-positives and about 2% of black HIV-positives.

(F) Table 2, HAART saves lives — but doesn’t prolong them!?, 17 September 2008

Posted in HIV absurdities, HIV and race, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests, HIV varies with age, HIV/AIDS numbers, M/F ratios | Tagged: , | 9 Comments »


Posted by Henry Bauer on 2008/05/02

A clear disproof of HIV/AIDS theory is the fact that the demographics of “HIV-positive” are constant: the geographic distribution has not changed in two decades, neither has the rate at which people test positive; and the racial disparities have remained the same. The numbers given in my book continue to be replicated by other and by later reports, see for example REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”, 1 April 2008. The latest report on “HIV” in prisons once again replicates salient trends:

The overall rate of “HIV-positive” in prisons, 2004-2006, was 1.7-1.8%; most of the cited sources in my book reported 2-3%. More strikingly, the geographic distribution is once again the same: Northeast (3.9%) > South (2.2%) > Midwest (0.9%) and West (0.7%).

The same geographic distribution is seen among prisoners as among military cohorts including applicants, new mothers, blood donors, members of the Job Corps, and the totality of public testing sites. The geographic distribution of “HIV-positive”, in other words, is not a function of social status or circumstances, and it is not a function of time, having remained without significant change for more than twenty years.

Moreover, the geographic distribution can be calculated simply from the racial disparities in testing “HIV-positive” and the racial composition of the population in each region (DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008).

“HIV-positive” is not the mark of an infectious agent.

Posted in HIV and race, HIV does not cause AIDS, HIV tests, HIV transmission, HIV/AIDS numbers | Tagged: , | 2 Comments »

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