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

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 http://www.omsj.org/human-rights/52nd 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.

 

“HIV” is NOT sexually transmitted — yet more clear evidence

Recent Nobelist in biology, Randy Schekman, launched a venture to improve publication of valuable research (Science rewards hucksters and spin artists, not soundly tested science): the Open Access on-line eLIFE.

Straightforward evidence that “HIV” is not sexually transmitted — in particular, not by heterosexual intercourse in Africa — is present in “Earlier menarche is associated with a higher prevalence of Herpes simplex type-2 (HSV-2) in young women in rural Malawi”, Glynn et al., eLife 2014;3:e01604, 28 January 2014.

The article’s main point is less than surprising: “girls with earlier menarche tend to have earlier sexual debut and school drop-out, so an association might be expected” with being more likely to contract sexually transmitted infections (STIs or STDs).
That expectation was confirmed by a close-to-linear relationship between age at menarche and prevalence of herpes (HSV-2) infection:

By contrast, there was no correlation at all between “HIV-positive” and age at menarche.

Furthermore, prevalence of “HIV” was much lower than that of HSV-2, contrary to yet another shibboleth of HIV/AIDS theory, namely, that infections by an STD like HSV-2 makes “HIV-positive” more likely:

In an earlier article (Glynn et al., “Assessing the validity of sexual behaviour reports in a whole population survey in rural Malawi”, PLoSONE, 27 July 2011) the ratio of “HIV-positive” to HSV-2 infection had been reported as 4/31 for females and 2/52 for males, again confirming that “HIV-positive” is much less prevalent than HSV-2.

Not, of course, that this further evidence that “HIV” isn’t an STD will make any difference, more-than-ample evidence has been around for many years.

Census Bureau supports Duesberg

Duesberg et al. (“HIV-AIDS hypothesis out of touch with South African AIDS – A new perspective”)  had debunked the claim by Chigwedere, Essex, et al. (“Estimating the lost benefits of antiretroviral
drug use in South Africa”, JAIDS 49 [2008] 410-5) that antiretroviral treatment could have saved about 330,000 lives in South Africa between 2000 and 2005 — or 2.2 million person-years — were it not for the misguided theories of Peter Duesberg taken seriously by President Mbeki.
So threatening to the HIV/AIDS Establishment was the Duesberg refutation of Chigwedere et al. that Nobelist Barre-Sinoussi was enlisted to lead-sign a protest against the Duesberg publication, which led eventually to the demise of Medical Hypotheses as a credible vehicle for innovative ideas (“Elsevier-Gate”): the journal’s new editor claimed it possible both to  “publish radical new ideas” and at the same time “not . . .  get into controversial subjects” (Martin Enserink, “New Medical Hypotheses editor promises not to stir up controversy”, ScienceInsider, 25 June 2010).
Duesberg et al. had resorted to Medical Hypotheses only after JAIDS — the journal that had published the Chigwedere article — had refused, counter to all standard practice not to say common decency, to allow a response in  its own pages.
Despite Elsevier’s withdrawal of the Duesberg article, it has been freely available  on the Internet, but it seemed proper and useful to have it in the mainstream literature indexed as other than “withdrawn”. Independent peer review led to the recent publication of the Duesberg arguments in the Italian Journal of Anatomy and Embryology , and the abstract is now in PubMed:

Of course the HIV/AIDS vigilantes were beside themselves at this turn of events, and even more that it was brought to widespread attention by a piece on the Nature website. Subsequent fury was expressed in comments to that piece, leading to rather comical machinations by Nature editors attempting to cleanse its site by “losing” those comments owing to an alleged software glitch, see “NATURE and science journalism”.
That blog posting brought a highly informative comment  from Jean Umber: Dr. Willy Rozenbaum, who had given Montagnier the first samples in which “HIV” was supposedly found, had published in 2007 a presentation which showed projections by the US Census Bureau of how the population of South Africa would grow if AIDS were present or if AIDS had not been present:

This is precisely one of the arguments made by Duesberg et al., that the actual population growth in South Africa is what had been projected to happen if AIDS were not present:

According to the official doomsayers of the HIV/AIDS faith, AIDS should have capped the South African population at about 45 million around the year 2000; instead the population has continued to grow in steady fashion.
The defenders of HIV/AIDS theory had ventured a couple of substantive criticisms of the original Duesberg article, among them that this comparison of actual with projected population growth is not convincing. Yet it is the US Census Bureau that published the projections with and without AIDS, and what actually happened is precisely what the Bureau projected if AIDS were not decimating the population.
Rozenbaum’s slide does not give details (other than the date of 2004) for the actual Census Bureau documents from which he extracted these projections. It may well have been The AIDS Pandemic in  the 21st  Century, issued March 2004, tagged WP/02-2, described as an International Population Report by  Karen A. Stanecki, and given the imprimatur not only of the US Census Bureau but also of the Office of HIV/AIDS, Bureau for Global Health, U.S. Agency for International Development. That document does give copious details of projections with and without AIDS, in numbers and histograms and graphs. It also provides even further support for the validity of the case made by Duesberg et al.:
One of the persistent criticisms made by HIV/AIDS vigilantes is that numbers for the prevalence of “HIV-positive” used by Duesberg et al. came from pre-natal clinics and that data on pregnant women was not a valid proxy for the rate of “HIV-positive” in the general population of South Africa. To the contrary, the Census Bureau points out that it is a very good proxy, and why that is the case:

Although this particular figure refers to data from Zambia, the Census Bureau describes it as representative for all of sub-Saharan Africa:
“In Sub-Saharan Africa,  More Women Than Men  Are HIV Positive
At the end of 2001, UNAIDS estimated that 58 percent of all HIV infections in Sub-Saharan Africa were among women.  Peak HIV prevalence among women occurs at a younger age than among men: around age 25 compared to age 35-40.  As Figures 3 and 4 show for Rwanda and Zambia, younger women tend to have higher levels of HIV infection than men of their same age. Several studies have shown that HIV prevalence among pregnant women attending antenatal clinics provides a reasonable overall estimate of HIV prevalence in the general adult population, although it underestimates the rate among all women while overestimating it among men.  This is shown for Zambia in Figure 4.”

*                    *                    *                    *                    *                    *                    *                    *

Note that the Census Bureau Figure 4 above is also yet another illustration of the demographic fact that, in all populations for which data have been published, prevalence of “HIV-positive” rises from the mid-teens and falls again at higher ages, and that females test “HIV-positive” more than males at the younger ages while the opposite is seen at higher ages. The exact ages at which the ratio reverses, and at which “HIV-positive” reaches a maximum, varies not only with sex but also with race; African genes are associated with a longer age-span during which females test positive more than males. For details see a number of earlier blog posts confirming all the trends pointed to in The Origin, Persistence and Failings of HIV/AIDS Theory.

Youngest person sexually infected with HIV? How are pre-teens infected?

“Teenaged boy contracted HIV through intercourse — A 13-year-old boy has become the youngest patient to contract HIV through sexual intercourse, health officials said. It is suspected the boy became infected while working part-time for a 50-year-old male, who used money to lure him into having sex, Centers for Disease Control (CDC) Deputy Director-General Lin Ting . . . said”.
This report is from China (Taiwan), but the same sort of nonsense could have come from anywhere.
The demographic characteristics of “HIV” — that is, of testing “HIV-positive” — make quite plain that “HIV” is not an infectious agent, let alone a sexually transmitted one. The evidence for that is set out in considerable detail in The Origin, Persistence and Failings of HIV/AIDS Theory, and more such evidence has been presented many times on this blog.
Consider the data from the Centers for Disease Control and Prevention from all public testing sites in the USA for the period 1995-98, as published in The Origin, Persistence and Failings of HIV/AIDS Theory [“F(HIV)” means the frequency of positive “HIV” tests, a term I used to avoid speaking about “HIV infection” or “HIV prevalence”]:

Now ask,

How did those people of various ages
become “HIV-positive”?
In particular, ages up to the teens?

At birth, babies carry antibodies generated by their mothers; 75% or more of “HIV-positive” babies got their “HIV” antibodies direct from their mothers, and lose them in less than a year; see  “Mother to child transmission of HIV and its prevention with AZT and Nevirapine — a critical  analysis  of  the  evidence” (2001) by the  Perth  Group, available at www.theperthgroup.com/monograph.html.
By age 1, let alone ages between 1 and 12, babies and young children can therefore be “HIV-positive” only for some other reason than maternal antibodies. What could that reason be?
Note that the rate of “HIV-positive” continues to decline into the early teens. That was not owing to deaths reducing the number of “HIV-positives”, because in the 1990s no appreciable number of American babies or young children were dying of “HIV disease”.
Mother-to-child “transmission of HIV”, including via breast milk, had essentially ceased in the USA by the 1990s, so the only remaining means of infection would have been sexual transmission, dirty needles, or transfusion with contaminated blood. But, again, in the USA the two latter modes were almost unheard of by the mid-1990s, and sexual transmission (via sexual abuse, of course) is incredible at such high rates.
In any case, actual “infection” by any mechanism at all could not be the reason why these pre-teens tested “HIV-positive” since the rate of “HIV-positive” declined steadily, reaching a minimum in the low teens, and could not have been owing to deaths, as already remarked.
The only feasible explanation for the manner in which “HIV-positive” varies with age from birth into the teens is that testing  “HIV-positive” represents detection of substances that are associated with physiological stress, not an infectious agent. Birth is stressful, and children become physiologically stronger as their immune systems develop increasingly for years after birth. The Perth Group has published copious evidence that “HIV” tests are sensitive to and tend to test positive in the presence of oxidative stress.
That conclusion is underscored by the fact that the same variation of “HIV-positive” with age was found in healthy African subjects:

As a number of other posts on this blog have also illustrated, the manner in which “HIV-positive” varies with age is the same wherever and whenever such data are gathered, though the exact ages of the maxima and minima vary somewhat, in particular by race.

“HIV” tests do not detect a human immunodeficiency virus,
as consideration of the tests themselves already shows:
“HIV tests are not HIV tests”.

The mistaken belief that testing “HIV-positive” represents infection by a sexually transmitted agent has led to innumerable tragedies for some uncountable number of people: for instance, being needlessly fed toxic drugs, or being incarcerated for supposedly spreading a deadly infection, or becoming depressed upon being told that one is infected.

World AIDS Day: Black Stars and “life-saving” HAART

Those who address primarily African-American audiences about “HIV/AIDS” have an impossible task, because “HIV/AIDS” in the United States has become concentrated among blacks, and that fact combines with the mainstream view of how “HIV” spreads to resuscitate or re-emphasize old stereotypes of unrestrained irresponsible sexual behavior by black people.
The standard assertion that “stigma” must be removed from being “HIV-positive” is whistling in the wind, when the same voices that decry stigmatization ascribe being “HIV-positive” to “down-low” cheating on female partners, injecting illegal drugs with dirty needles, failing to use condoms, having multiple concurrent sexual relationships, and incessantly changing partners.
The self-contradiction leads to extraordinary pseudo-intellectual contortions like those of Adimora et al. described in “Facts versus Faith (cognitive dissonance again)”.

On the occasion of World AIDS Day, the website Black Voices paid tribute to outstanding black high-achievers lost to HIV/AIDS. Here is their list, sub-divided [by me] into pre-HAART (<1996) deaths and post-HAART deaths:
Pre-HAART:
Alvin Ailey — Famed choreographer . . .  died at the age of 58 years old in 1989
Arthur Ashe . . . . worked tirelessly . . .  [with] AIDS Awareness from 1992 — when he revealed the illness — until his death on Feb.6, 1993. [Born 1943; by-pass 1979, heart surgery 1983, ill 1988 and tested “HIV-positive”, presumed from transfusion in 1983; had talked about stopping AZT not long before he died]
Eazy E . . . . died one month after being diagnosed with AIDS at 31 years on March 26, 1995.
Max Robinson . . . . died Dec. 20, 1988 at age 49.
Howard Rollins . . . got into trouble with the law and battled both drug habits [my emphasis] and a myriad of legal issues. . . . died on Dec.8, 1996. [born 1950]
Willi Smith . . . . [died] at age 39 [in 1987]
Sylvester . . . . gay, cross-dressing vocal powerhouse born as Sylvester James. . . . dying in San Francisco in 1988. [born 1947]
Post HAART:
Kenny Greene . . . . Before his passing, at age 32, Greene opened up to Sister 2 Sister magazine in 2001 admitting that he was suffering from AIDS and revealed he was bisexual.
Fela Kuti . . .  Nigerian singer and songwriter . . . . infamously married upwards to 27 women in a single ceremony in 1978. [Born 1938; died 1997 of KS]
Gene Anthony Rae . . . . suffering a stroke in 2003.  He died at age 41.
Jermaine Stewart . . . . died March 17, 1997 at the age of 39.

This adds a small amount of data to the mass of evidence debunking the claim that HAART is life-saving: here are the ages of death pre- and post-HAART:
Pre-HAART:  58; 50; 31; 49; 46; 39; 41   AVERAGE   =  45
Post HAART:  32; 59; 41; 39                    AVERAGE   =  43

Note once again, too, how “HIV” and “AIDS” — uniquely — most affects people in the robust adult years of young-middle-age [No HIV “latent period”: dotting i’s and crossing t’s, 21 September 2008].

Several Internet sources, including some maintained by Bristol-Myers-Squibb, recently featured a black poster-woman for life-saving HAART:
“Despite having neuropathy, a condition caused by her HIV medications that has damaged the nerves in her legs and leaves them feeling numb, Davis, 51, has raised money for Harlem United by completing the New York City Marathon twice”
— Woman with HIV/AIDS preaches compassion.
“Maria Davis was devastated when she learned she was HIV-positive. . . . In 1995 Maria’s life took a turn, she contracted the HIV virus unknowingly from her soon-to-be-husband”
— National Black Leadership Commission on AIDS.
“In 1995, Maria Davis learned she was infected with HIV. The diagnosis was especially hard on her two children”
— Bristol-Myers-Squibb.
As usual, crucial details are missing, for instance the “HIV” status of her children and their father. It would, however, be typical if it had simply been inferred that the father must have been the source of Maria’s “HIV”, even though many studies in Africa have reported that pregnancy can cause “HIV-positive” status and multiple pregnancies can leave a woman permanently “HIV-positive”. It would also be typical if this presumption had led to the break-up of an otherwise stable partnership (see, for example, p. 77 ff. and p. 247  in The Origin, Persistence and Failings of HIV/AIDS Theory).
It is atypically honest, however, that neuropathy is ascribed so unequivocally to HAART.