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 on the Internet, but it seemed proper and useful to have it in the mainstream literature indexed as other than “withdrawn”.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.

GAYnocide in San Francisco

In “Predicting rates of ‘HIV-positive’ — and racial cleansing” (2010/03/14), I pointed out that Washington DC was setting out on an unwitting campaign of racial cleansing: testing everyone for HIV and administering toxic drugs to all “HIV-positive” people, irrespective of their state of health, would lead to a disproportionate number of African Americans being killed by the toxic drugs, since black people test “HIV-positive” far more often than others.

Now San Francisco is setting out to cleanse itself of gay men in the same manner:
“City endorses new policy for treatment of H.I.V.” (2 April 2010, Sabin Russell)

“San Francisco public health doctors have begun to advise patients to start taking antiviral medicines as soon as they are found to be infected . . . . The new, controversial city guidelines, to be announced next week by the Department of Public Health, may be the most forceful anywhere in their endorsement of early treatment against H.I.V., the virus that causes AIDS. . . . Behind the policy switch is mounting evidence that patients who start early are more likely to live longer, and less likely to suffer a variety of ailments — including heart disease, kidney failure and cancer — that plague long-term survivors.”
As I’ve pointed out before, perfectly healthy people take longer to be killed by toxic drugs than people who are already ill. Testing “HIV-positive” can result from a huge variety of different conditions. Among gay men, one prominent cause may be the practice of rectal douching, which can damage the intestinal microflora that constitute a significant arm of the immune system, acting in particular to control fungal infections — see Tony Lance’s hypothesis of intestinal dysbiosis and his presentation at RA 2009, now available in video format (most conveniently on YouTube).
People who test “HIV-positive” AND have symptoms of illness are surely less healthy than people who test “HIV-positive” and do NOT have symptoms of illness. Up to now, therefore, the less healthy people are, the more immediately they have been put on antiretroviral treatment, and therefore they have died sooner from the drugs’ “side” effects than those who start HAART while they are more healthy. We already know that the majority of adverse events among people on HAART are “non-AIDS” events — “side” effects of the treatment that result in organ failure [NIH Treatment Guidelines, 29 January 2008, p. 13; ; p. 21, November 2008].

The first thing that any “HIV-positive” person should do
is to try to discover WHY they are testing “HIV-positive”:

Have they recently taken antibiotics? Have they recently had surgery? Been pregnant? Had an anti-tetanus shot? A flu shot? Do they eat healthily and eschew douching? And so on. Almost any unusual physical condition appears able sometimes to stimulate a positive “HIV” test — certainly the use of “recreational” drugs and thereby probably the intake of significant amounts of other drugs as well.

The “variety of ailments — including heart disease, kidney failure and cancer — that plague long-term survivors” do NOT plague long-term non-progressors. Those adverse events were never suffered by AIDS patients in the 1980s, that has happened only since the introduction of antiretroviral drugs. Those ailments — “non-AIDS events” as the NIH Treatment Guidelines classes them — plague long-term HAART-treated “survivors”.

“Studies suggest that in the early years of infection, when a patient may show few signs of immune system failure, the virus is in fact causing permanent damage that becomes evident later.”
“Studies suggest” that only because it is assumed, without any direct evidence, that “HIV” somehow damages every cell in the body — magically, since it has never been found in any cells to any significant degree. Demonstrably “infected” people’s CD4 cells, the purported primary target, are “infected” at a rate of much less than 1%, after all (references cited at p. 176 in Duesberg, Inventing the AIDS Virus).

“For instance, in older patients who finally start taking the drugs, the effects of chronic inflammation take their toll.”
Re “older”: Bear in mind that everything about HIV/AIDS is at a maximum in early middle age, 35-50. There is no indication at all of the postulated latent period, and the mortality of PWAs (People With AIDS) does not increase with age, even as mortality from every other known cause increases dramatically with age above the middle years. In 2004, for example, the mortality of PWAs ≥65 was 1.8% whereas that at ages 25-34 was 1.7%, at 35-44 3.2%, at 45-54 3.8%, and at 55-64 2.6% [How “AIDS Deaths” and “HIV Infections” Vary with Age — and WHY, 15 September 2008; HAART saves lives — but doesn’t prolong them!?, 17 September 2008;  No HIV “latent period”: dotting i’s and crossing t’s, 21 September 2008; Living with HIV; Dying from What?, 10 December 2008]
The “chronic inflammation” is a pure guess. Since it has never been discovered just how “HIV” supposedly kills the immune system, a popular guess nowadays is that it must cause chronic inflammation, chronic stimulation of the immune system, which then by some unknown mechanism destroys itself — even though an earlier speculation that AIDS is an autoimmune disease turned out to be wrong. The logic of “chronic inflammation” is analogous to the invention of the term “immune restoration syndrome” to describe the finding that recovery of CD4 counts and diminution of “viral load” was often accompanied by severe illness or death on the part of the fortunate patient whose treatment had been so successful.
Bear in mind, too, that these speculations about chronic inflammation and the like are largely based on observation of HAART-treated individuals, or at least individuals who are not only “HIV-positive” but also in poor health, because most healthy untreated “HIV-positive” individuals are not being monitored. Long-term non-progressors or elite controllers have remained perfectly healthy for as long as a quarter century while “HIV-positive”, and since they are healthy, their existence as “HIV-positive” has never come to official attention. By contrast, it is beginning to be noticed that HAART produces premature aging [“Another kind of AIDS crisis”, David France, 2009/11/01].

“Dr. Diane V. Havlir, chief of the H.I.V./AIDS division at San Francisco General Hospital, said the new policy was already in effect for her patients. Although a decision whether or not to take the medicine rests with the patient, all those testing positive for H.I.V. will be offered combination therapy, with advice to pursue it.”
How many of her patients have had the opportunity to hear the reasons offered by Rethinkers for not starting HAART?

“The turning point in San Francisco’s thinking may have been a study in The New England Journal of Medicine on April 1, 2009, that . . . found that patients who put off therapy until their immune system showed signs of damage had a nearly twofold greater risk of dying — from any cause — than those who started treatment when their T-cell counts were above 500.”
Exactly. Those who were ill “from any cause” when they started HAART were twice as likely to die as those who were not ill when they started taking the toxic drugs. What a surprise!

“When the first combinations of AIDS drugs came out in 1996, the thinking was ‘hit early, and hit hard.’ But as patients battled nasty side effects, like diarrhea and disfiguring shifts in body fat, therapy was deferred until T-cell counts fell as low as 200. Today, with safer drugs, quick viral suppression is back in fashion.”
“Safer” drugs does not mean safe, of course. Just read the NIH Treatment Guidelines.

“The field is moving, inexorably, to earlier and earlier therapy,” said Dr. Anthony Fauci, director of the National Institutes for Allergy and Infectious Diseases. He called San Francisco’s decision “an important step in that direction.”
Connoisseurs of bureaucratese will recognize the passive voice of “The field is moving, inexorably” as the typical maneuver designed to disclaim responsibility for decisions being made or influenced by the person who deploys the passive-voice statement. “Mistakes were made” is a common enough example; they just happen, no one committed them.
And this “inexorable” move is actually opposed by some highly qualified HIV/AIDS experts like “Jay Levy, the U.C.S.F. virologist who was among the first to identify the cause of AIDS”, who commented that “It’s just too risky”; “The new drugs may be less toxic, . . . but no one knows the effects of taking them for decades”.
“San Francisco’s decision follows a split vote in December by a 38-member federal panel on treatment guidelines. Only half of the H.I.V. experts gathered by the Department of Health and Human Services favored starting drugs in patients with healthy levels of more than 500 T-cells. . . . The risks of early treatment — giving powerful drugs to people at low risk of disease — could outweigh the ‘modest predicted benefit’ . . . . Dr. Lisa C. Capaldini, who runs an AIDS practice in the Castro district, also has strong reservations. . . . [Although] today’s drugs are a vast improvement over earlier therapies, the program, she said ‘is not ready for prime time.’”

But San Francisco pushes ahead,
“advising” everyone to get tested
and “advising” all “HIV-positive” people
to start treatment immediately,
thereby preparing for
genocide of gay men in San Francisco
to accompany
genocide of African Americans in Washington DC

Doctors, nurses, dentists: Why no risk from HIV?

The assertion that AIDS is caused by an infectious agent brought widespread panic, as anyone with memories of the 1980s can testify. As soon as HIV tests became available, everyone entering a hospital was asked to give “informed consent” to be tested. Teenagers were advised to get their prospective partners tested before having sex. Dentists started to wear masks and to put on new gloves in demonstrative fashion with each new patient. Police had themselves tested if any body fluids from another person came into contact with them, and some people were arrested and charged with attempting to infect others through spitting on them.

Eventually it was recognized that toilet seats were not a transmission route for HIV, and that the risk of contracting HIV via saliva — kissing, oral sex — was negligible. Those facts were not broadcast as continuously and intensively as the initial panicky warnings, though, so even now there are people who believe that “HIV” is readily acquired by almost any contact with almost anything from an “HIV-positive” individual.

Naturally, then, doctors and nurses were regarded as being at high risk from accidental contact with contaminated blood or other fluids, and there were occasional reports of apparent infection of healthcare workers, for example through accidental needle-stick. However, over the years and decades it became clear that doctors, nurses, medical orderlies, etc., are NOT at any perceivable risk of acquiring “HIV” — see sources cited at pp. 47-8 in The Origin, Persistence and Failings of HIV/AIDS Theory. What remains are “urban legends” that will not die, like “the Florida dentist” who supposedly infected 5 of his patients, notably Kimberley Bergalis who subsequently died. In point of fact, that particular story has been thoroughly debunked by, for example, Root-Bernstein (pp. 46-7, 314-5 in Rethinking AIDS, 1993) and Stephen Barr (“Perspective: The 1990 Florida dental investigation: is the case really closed?”, Annals of Internal Medicine 124 [1996] 250-4). Bergalis died in a few short years of treatment with high-dosage AZT.

I was just alerted to an article I had not known about before, recalling in 2004 that dentists, too, have been found to be at no occupational risk of catching “HIV” or “AIDS” — E. J. Neiburger (Director, Center for Dental AIDS Research), “Dentists do not get occupational AIDS: An open letter to the profession — an evidence-based study on the AIDS epidemic in dentistry”, Journal of the American Association of Forensic Dentists, 26, #1-3, 2004:
“There are [not] (and never have been) any documented cases of dental workers getting occupational HIV/AIDS. (1, 2).”
(1) CDC. Health care workers with documented and possible occupationally acquired AIDS/HIV infection, by occupation, reported through June 2000, United States. HIV/AIDS Surveillance Report 2001;12(1):24.
(2) Department of Labor-OSHA. Occupational exposure to bloodborne pathogens: final rule. Federal Register 1991;57 (235):64005-64157.

Incidentally Neiburger cites examples of how the Centers for Disease Control and Prevention (CDC) exaggerates HIV/AIDS numbers, and he discusses CDC’s badly flawed actions concerning “the Florida dentist”. He points out that CDC likes to focus on the 25-44 age group because that’s where HIV/AIDS numbers and percentages are highest — remember that EVERYTHING about “HIV” and “AIDS” is at a maximum in that age range: age of first “HIV infection”, of first “HIV” test, of first “AIDS” diagnosis, and of deaths from “AIDS” or “HIV disease”. There’s no sign of the alleged latent period of a decade between “infection” and illness; and unlike any other disease, let alone an infectious one, let alone a sexually transmitted one, HIV/AIDS affects maximally adults in the prime years of life — “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 and Surgeons, 13 [2008] 77-81; “No HIV ‘latent period’: dotting i’s and crossing t’s”, 21 September 2008; “HAART saves lives — but doesn’t prolong them!?”, 17 September 2008; “How ‘AIDS deaths’ and ‘HIV infections’ vary with age — and WHY”, 15 September 2008.  Older people are less able to withstand any sort of stress, so death rates increase with age — except with “HIV/AIDS” (Table 1, “Age shall not wither them — because HIV really doesn’t kill”, 4 February 2009). Sexually transmitted infections are most common in teenagers and young adults.
The Neiburger article also cites interesting studies of how commonly people lie when asked about high-risk behavior. It mentions false-positive “HIV” tests but cites only a tiny portion of the supporting material. There are a few careless errors, like 1944 for a 1994 reference or Secretary Shalala instead of Secretary Heckler. But the meat of the piece, fully source-documented, is a deconstruction of the 7 cases mentioned by CDC as “’possible’ occupational HIV/AIDS transmission”. Overall, it’s evident that the designation “possible” should really have been “could not be ruled out”, because there were no positive data supporting transmission, just the observation that the dentists were “HIV-positive” in absence of definitively known personal risk factors.
In sum: There is not a single demonstrated case of a dental worker infected occupationally with “HIV”.

That does not prevent “researchers” from asserting, though, that “HIV transmission in the dental care setting continues to be of concern”. In an article published 2 years after Neiburger’s, Scully & Greenspan (Journal of Dental Research, 85 [2006] 794) make that assertion and cite Neiburger only for his mention of two “possible” cases, without telling readers of his deconstruction of those two cases. Further, Scully & Greenspan discuss “the Florida dentist” without even mentioning Barr or Root-Bernstein and their deconstructions, and Scully & Greenspan refer to “genetic similarity” as supporting evidence of transmission even though Barr had discovered, based on publications in Nature, “potentially serious flaws in the phylogenetic analyses used by the CDC to conclude that the dentist and his patients had the same strain of HIV”.
Here we have yet another example of a “peer-reviewed” publication that fails to mention centrally important prior publications. It is not overly cynical, I suggest, not in any way unfaithful to the facts, to recognize that any manuscript about HIV/AIDS whose conclusions fit the mainstream view of an ever-present danger will receive merely cursory “peer review” and approval, while manuscripts questioning the mainstream view are rejected irrespective of their substantive claims. Thus Duesberg has tried to point out that the Statistician General of South Africa has discussed in detail why the official count of about ~15,000 AIDS deaths per year is likely to be accurate within some tens of percent and why the estimates made by the Medical Research Council and UNAIDS of >300,000 is unacceptable; yet JAIDS, which published a political diatribe accusing President Mbeki , and by implication Duesberg, of guilt for some of those “300,000” deaths, refused to publish Duesberg’s correction, and in rejecting it did not even mention the official count of ~15,000 or the Statistician General’s published support for it, let alone argue why they should be ignored.

Bad as all that is, it’s still a subsidiary point compared to the mountain of evidence that “HIV” is not a transmissible infectious agent, illustrated for example by the fact that healthcare workers are at no occupational risk of acquiring “HIV”.
(Of course, the condition of “HIV-positive” may occasionally be contagious, in those circumstances where “HIV-positive” stems from a false-positive “HIV” test occasioned by such infectious agents as Epstein-Barr virus, flu, hepatitis, herpes, syphilis, or others that have been reported to cross-react on “HIV” tests.)