Lessons from the “baby cure”

ABC News has an unusually well researched, insightful discussion by Sydney Lupkin of the much-ballyhooed alleged cure of an HIV-infected baby: “Experts question so-called HIV ‘cure’”.

The chief points raised are about lack of proof of infection and questions of informed consent. But I would like to point to some deeper issues in medical practice: doctors’ dilemmas and doctors’ ignorance.

“Caplan [medical-ethics specialist] and Kline [pediatric HIV specialist] said they believe Gay [the doctor responsible for the ‘cure’] had the patient’s interests at heart, and that she had the right to deviate from standard of care”.
Having a patient’s interest at heart is no more than the good intentions that, in general, pave the road to hell. Good intentions coupled with technical ignorance can have horrible consequences. Furthermore, human psychology being what it is, one’s belief to be acting with good intentions may not be well based if one suffers the usual conflicts of interest, say, wanting to demonstrate expertise.

“‘When we consider starting any medication in any patient, we always consider the risk-benefit ratio,’ Gay said during Monday’s press conference. ‘When the risk is something as serious as HIV disease, then it’s worth the benefit that you may get from preventing that disease. Even though you never want to start drugs that may cause toxicities, if the benefit outweighs the risk, you do it.’”
“Risk-benefit”, like “evidence-based medicine”, are phrases that can lull the unwary into believing that things are being done to the highest scientific standards.
But “evidence-based medicine” is a hope, a motto, an (impossible?) ideal, it is not a description of current practices, few if any of which are actually based on evidence; for example, innumerable people, are taking drugs to lower cholesterol or blood pressure and increase bone strength, yet “There are no valid data on the effectiveness . . . [of] statins, antihypertensives, and bisphosphanates” (the last, e.g. Fosamax, are prescribed against osteoporosis) — Järvinen et al., British Medical Journal, 342 (2011) doi: 10.1136/bmj.d2175.
As to “risk-benefit”, that sounds like a careful weighing of quantitative statistical data, when in practice — as in the baby-cure case — it’s no more than a subjective guess.

Ignorance about HIV/AIDS is the current “standard of care”, sadly.

For example, “transmission-reducing drugs during pregnancy . . . have been found to reduce the rate of HIV transmission to 1 percent, said Dr. Mark Kline, a pediatric HIV and AIDS specialist at Baylor College of Medicine in Houston. Without these prenatal preventive measures, babies have a 20 to 25 percent chance of becoming infected with their mother’s HIV”
— but those authoritative, impressive-appearing percentages are based, like all else about HIV, on tests that are simply not valid. Once more:

 THERE   ARE   NO   “HIV”   TESTS
 CAPABLE   OF   DIAGNOSING
 ACTUAL   INFECTION

—— S. H. Weiss & E. P. Cowan,
 “Laboratory Detection of Human Retroviral Infection”,
 Chapter 8 in Gary P. Wormser (ed.),
 AIDS and Other Manifestations of HIV Infection, 2004 (4th ed.).

The truth is hidden in plain sight, obscured only by cognitive dissonance. Thus Kline, who gets so much right — if only the premises were not wrong — apparently has not thought seriously about the implications of the absurdities  and conundrums that pervade HIV/AIDS theory:
“‘That’s a rather surprising statistic, I think, because you think to yourself: If the mother has HIV, won’t the newborn almost certainly also have HIV?’ Kline said. ‘In fact, even in an era in which we did nothing at all, only minor numbers of infants actually acquired HIV infection.’”

Exactly. Just as this supposedly sexually transmitted disease that supposedly galloped through southern Africa and elsewhere is, in the words of Gallo himself, “distinctively [sic] difficult to transmit” (Robert Gallo, Virus Hunting: AIDS, Cancer, and the Human Retrovirus: A Story of Scientific Discovery, Basic Books, 1991, p. 131);
and the officially claimed HIV+ rate in southern Africa can only be explained by postulating promiscuity so extraordinary that people could hardly have time for anything except sex and changing partners: James Chin, former epidemiologist for California and the World Health Organization, calculates that 20-40% of adults must have “multiple concurrent relationships” with several sexual partners, changing to new partners weekly or monthly, totaling to tens of different partners over the course of each year (The AIDS Pandemic, Radcliffe 2007, Table 5.1 on p. 64).

Surely the colossally mind-boggling absurdities and self-contradictions required by HIV/AIDS theory call for the most careful reconsideration of that theory; and reconsideration might bring to the fore the fact that “HIV” virions have never been isolated from patients even during so-called viremia when HIV is supposedly plentiful; and in absence of a sample of such virions, there cannot be a “gold standard” test to validate currently used tests. As Rodney Richards has pointed out, the so-called “HIV” tests are actually “AIDS” tests and have never been shown by evidence, only by official opinion, to show infection by HIV ( “The birth of antibodies equal infection”, Appendix II in Celia Farber, Serious Adverse Events, Melville House, 2006). “HIV” tests react positive when sera contain some of the things found in AIDS patients BUT  NOT  ONLY  IN  AIDS  PATIENTS  NOR  IN  ALL  AIDS  PATIENTS: several dozen conditions are capable of producing a positive “HIV” test, for instance such common diseases (in Africa) as tuberculosis (Christine Johnson, “Whose antibodies are they anyway? Factors known to cause false positive HIV antibody test results”, Continuum 4 (#3, Sept./Oct. 1996); also Figure 22, p. 83 in The Origin, Persistence and Failings of HIV/AIDS Theory).

When Dr. Gay talked of “something as serious as HIV disease”, her belief was based in large part on the fact that, since the introduction of antiretroviral drugs, “HIV” is being held responsible for all the “side” effects of the drugs; for instance the mal-distribution of fat caused primarily by protease inhibitors (PIs) is often referred to as “HIV lipodystrophy”  as though HIV and not the PIs were at fault.

In the abstract I can sympathize with doctors who follow official guidelines and believe they are doing right by their patients. In practice I am appalled at the human carnage consequent on stubborn adherence to an unsupportable theory, which remains unquestioned by innumerable so-called “researchers” even as contradictions of the theory crop up all the time. And I find myself unable to comprehend the mindset of practicing physicians who continue to administer “medications” to babies even when the result is screaming and convulsions; or the mindset of doctors supervising clinical trials where the drugs are so intolerable that they have to be forcibly administered via gastric tubes. Not to speak of the fanatics who try to justify such actions.

Antiretroviral drugs lead to normal life?

The advent of antiretroviral “cocktails”, combination antiretroviral therapy, HAART, is said to have made HIV/AIDS a manageable chronic disease to the extent that “HIV-positive” individuals can lead essentially normal lives for essentially normal life-spans — at least according to official statements repeated by the media from interviews with gurus and VIPs and from press releases put out by government agencies and by drug companies.

The technical literature, on the other hand, is replete with descriptions of highly unpleasant, health-threatening “side” effects from all antiretroviral drugs and combinations. Note for instance that the Treatment Guidelines  have been revised once or twice a year for well over a decade, and revisions are made on-line even more frequently, raising suspicions as to just when the treatment became so successful as to permit normal living and why recommendations have still needed to be revised so often.
Moreover, if treatments are so successful, what need is there for patients to “understand the . . . risks of therapy” [emphasis added] and to consider deferring therapy? (Treatment Guidelines, 27 March 2012 version, introductory pages):
“Patients starting ART should be willing and able to commit to treatment and should understand the benefits and risks of therapy and the importance of adherence . . . . Patients may choose to postpone therapy, and providers, on a case-by-case basis, may elect to defer therapy on the basis of clinical and/or psychosocial factors”.

One wonders, too, at such sections in the Guidelines as “What Not to Use: Table 8. Antiretroviral Regimens or Components That Should Not Be Offered At Any Time”.
This includes not only the NRTI monotherapy and Dual-NRTI therapy that was officially lauded from the late 1980s into the mid-1990s before being suddenly superseded. “What Not to Use” also lists a goodly number of combination therapies that were earlier recommended!

There are hints everywhere in these Guidelines that what was once recommended is to be avoided; for example, Table 8 includes such rather inscrutable comments as
“Clinicians caring for patients who are clinically stable on regimens containing TDF + ddI should consider altering the NRTIs to avoid this combination”: Obviously this earlier recommended treatment isn’t all that good. Some earlier combinations are now labeled “When no other ARV options are available and potential benefits outweigh the risks”: What risks? That one might lead a normal life?

“Adherence to treatment” qualifies for quite a bit of discussion in which “adverse drug effects” and “treatment fatigue” are mentioned only toward the end of a list that includes what some people (including me) might regard as nonsense, e.g. “low levels of health literacy . . . or numeracy (ability to understand numerical-related health information)”, which presumably means not believing what they are told when they complain of the debilitating effects of the treatment.

“Adverse Effects of Antiretroviral Agents” (pp. K7-11) documents that all antiretroviral drugs have such nasty “side” effects as “Bleeding events . . . Bone marrow suppression . . . Cardiovascular disease . . . Central nervous system (CNS) effects . . . Diabetes mellitus
(DM)/insulin resistance . . . Dyslipidemia . . . Gastrointestinal (GI) effects . . . Hepatic effects . . . Hypersensitivity reaction . . . Lactic acidosis (NRTIs, especially d4T, ZDV, and ddI ) . . . Lipodystrophy . . . Myopathy/elevated creatine phosphokinase . . . Nephrotoxicity/urolithiasis . . . Osteopenia/osteoporosis . . . Peripheral neuropathy . . . Rash (All NNRTIs) . . . Stevens-Johnson syndrome (SJS)/ toxic epidermal necrosis (TEN)”.
Here’s a thought experiment: How many people treated with these medications had to develop one of these “side” effects before it was noted and acknowledged? Keeping in mind that when an HIV/AIDS patient is being treated, deterioration in health is usually ascribed at first to “HIV”?

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This blog post was stimulated by a recent press release (31 December 2012) from the Food and Drug Administration: “FDA approves first anti-diarrheal drug for HIV/AIDS patients — Fulyzaq is the second botanical drug approved by the agency . . . . [It is to be used] to relieve symptoms of diarrhea in HIV/AIDS patients taking antiretroviral therapy . . . . Diarrhea is experienced by many HIV/AIDS patients and is a common reason why patients discontinue or switch their antiretroviral therapies. . . . The median number of daily watery bowel movements was 2.5” (emphasis added; hardly the normal life claimed in official propaganda).
A minor point of interest here is that a “botanical drug” is good when recommended by an official agency, but of course not when it comes from anyone who advises an “alternative” or “complementary” medical approach (“More mainstream alternative treatment for ‘HIV/AIDS’”).

The main general point I want to make is that one learns about the real effects of antiretroviral therapy only from reading between the lines of the official statements and looking into the underlying data. In particular,

continuing praise of new improvements in therapy
means inevitably that earlier treatments
 were less than completely satisfactory,
though that is never stated outright.

For example, that AZT did nothing beneficial and actually killed some proportion of patients has to be inferred from such hints as that it was omitted from estimates of how antiretroviral drugs had decreased mortality “[c]ompared with . . . untreated HIV disease” (“The survival benefits of AIDS treatment in the United States”, Walensky et al., Journal of Infectious Diseases 194 [2006] 11-19); or from noting that when AZT monotherapy was replaced by cocktails, there was an immediate halving  in mortality,  indicating that AZT had been responsible for about 150,000  deaths (“HAART saves lives — but doesn’t prolong them!?”).

The same point applies to how HIV tests are presented to the public, as reliable ways to diagnose infection (e.g. “‘HIV’ tests are self-fulfilling prophecies”; “‘HIV’ tests are demonstrably invalid”; “The Wonderland of ‘HIV’ ‘tests’”; “Health-threatening and life-threatening tests”). By contrast, the technical literature makes plain that no HIV tests or combination of tests can diagnose infection, given the lack of a gold-standard test (S. H. Weiss and E. P. Cowan, “Laboratory detection of human retroviral infection”, Chapter 8 in AIDS and Other Manifestations of HIV Infection, ed. G. P. Wormser, 2004). Straightforward calculations based entirely on official data show that at least half of the people who test positive on HIV tests will suffer no ill health on that account (“Iatrogenic harm following ‘HIV’ testing”, Journal of American Physicians and Surgeons 15 [#2, 2010] 42-6).

After many years of paying attention to these things, I remain astonished that public pronouncements by official agencies are so stunningly at odds with what is in the technical literature. One simply cannot rely on supposedly authoritative sources. Nor is that only my conclusion:

It is simply no longer possible to believe
 much of the clinical research that is published,
or to rely on the judgment of trusted physicians
 or authoritative medical guidelines.
I take no pleasure in this conclusion,
 which I reached slowly and reluctantly
over my two decades as an editor of
 The New England Journal of Medicine
—— Marcia Angell
“Drug companies and doctors: a story of corruption,”
New York Review of Books, 56 #1, 15 January 2009.

Why is HIV/AIDS a disease of black people?

“Throughout last month’s International AIDS Conference, HIV advocates highlighted the enormous disparities afflicting U.S. women of color, for whom HIV infection rates are skyrocketing and reaching levels similar to those of sub-Saharan Africa. . . . the rate of new HIV infections among black women was 15 times that of white women and over three times the rate among Hispanic/Latina women” — “HIV/AIDS Rates Rocket for Black U.S. Women”, ForbesWoman 8/13/2012.

Note first that the disparities are NOT enormous for “U.S. women of color”, only for black women, since they are affected 3 times as much as “Hispanic/Latina” women. Moreover, “Hispanic/Latina” is a highly artificial ethnic-linguistic category, within which genetically black people are affected by “HIV/AIDS” far more than whites: West-Coast “Hispanics”, who are largely Mexican, test “HIV-positive” at about the same rate as Native Americans and not much more than white Americans, whereas East-Coast “Hispanics”, who  are largely Caribbean and black, test “HIV-positive” at about the same rate as African Americans (see copious data from official sources cited in The Origin, Persistence and Failings of HIV/AIDS Theory).

As also shown in that book, the reason why black people test “HIV-positive” far more often than others — whites, Asians, Native Americans — is because the “HIV” tests are racially biased: something about the genetic haplotypes common in some sub-Saharan natives, probably related to the Bantu, produces a very high rate of testing “HIV-positive”.

But don’t go to the bother of looking at the data, which are conclusive. Just use common sense. Either African Americans and sub-Saharan natives share an inescapably determinative cultural or genetic proclivity for promiscuous and unsafe sex, or there is something physiological about their shared genetic ancestry that conduces to testing “HIV-positive” — bearing in mind that testing “HIV-positive” can result from innumerable conditions, including pregnancy or getting vaccinated.
The degree of promiscuous and unsafe sex needed to explain the “HIV” “pandemic” in sub-Saharan Africa has been calculated by Dr. James Chin, former epidemiologist for the World Health Organization and for California: 20-40% of adult Africans must be having about a dozen sexual partners at any given time and must be changing them about annually, to generate the network needed for the apparent “spread” of HIV (The AIDS Pandemic, 2007).

So which are you willing to believe?
That about one third of African Americans, women in particular, have about a dozen sexual partners at any given time, without practicing safe sex, and changing those partners about annually

 OR

  that there’s something about those highly non-specific “HIV” tests that responds to proteins commonly found in the sera of people with sub-Saharan genetic haplotypes?

Rewriting the Histories of AIDS and HIV

Public Broadcasting Service (PBS) likes to advertise itself as “the most trusted” something or other. Yet in July 2012 its FRONTLINE series featured a drastic and misleading rewriting of history in the program, “ENDGAME: AIDS IN BLACK AMERICA”, billed as “A groundbreaking two-hour exploration of one of the country’s most urgent, preventable health crises”.  This was written, produced, and directed by Renata Simone, who has been covering HIV/AIDS since 1987 and therefore had every opportunity to know better than to get crucial facts so wrong.
The central misdirection:
is a labored attempt to rewrite how AIDS has affected black Americans. AIDS has become essentially an African-American disease after beginning as essentially a gay disease affecting blacks to only about the extent to which they are present in the population as a whole. There has been a dramatic quantitative change from that beginning, and the reasons for it are quite clear: the re-definition of AIDS as requiring a positive HIV test and the fact that the tests are racially biased. ENDGAME, however, alleges that from the very beginning black Americans were affected by AIDS about as severely as they are now. That is plainly, undeniably wrong. Official numbers from the Centers for Disease Control and Prevention show that blacks accounted for less than 30% of AIDS cases in the early 1980s, but 60% by the end of the 1990s (MMWR  50 #21), and by 2010 black Americans were being diagnosed with AIDS at the rate of 43/100,000 compared to 4.4 for white Americans, 13.7 for Hispanics,  9.7 for Pacific Islanders, 7.2 for mainland Native Americans, and 3.5 for Asians (CDC Surveillance Report #22).
The labored case, that African Americans had been severely affected from the earliest days, had Dr. Michael Gottlieb saying that there were appreciable numbers of black Americans among early AIDS cases, it was just that no one thought to mention it; the first 5 were white, #6 was a Haitian, but #7 was an African American. Exactly: one out of seven, just as in the population as a whole; not, as in 2012, diagnosed at ten times the rate of diagnosis of white Americans; in 2010, Gottlieb would have seen 3 black AIDS cases for every 2 white case, not 1 in 7. Dr. David Ho seconds the view that appreciable numbers of AIDS cases were among African Americans, it just happened not to have been noted or reported anywhere, especially not to the CDC, apparently. Phill Wilson, founder and Executive Director of the Black AIDS Institute, asserts that gay African-Americans in Chicago just presumed AIDS was a West-Coast phenomenon — but it’s not at all clear how AIDS could not have been noticed in black communities in Chicago if appreciable numbers had been exhibiting the blatant symptoms of Kaposi’s sarcoma, thrush, and Pneumocystis carinii (now jiroveci) pneumonia. A lady in Oakland explains that gay blacks there, which is 45% black, didn’t talk about “HIV” in the early days whereas everyone was talking about it in San Francisco which has only 4% African Americans; and others support her opinion that it wasn’t talked about in Oakland because of certain features of black culture: keeping secrets, especially about being gay. But no one was talking about “HIV” in the early days (~1980-84), because it hadn’t yet been discovered; and, again, had AIDS been rampant, it would have been obvious.
Much of the nonsense in this program illustrates the damage done by taking HIV and AIDS as synonymous.
Iatrogenic harm to African Americans:
HIV/AIDS theory has caused inestimable damage to untold black Americans by breaking up relationships (see examples cited at p. 247 in The Origin, Persistence and Failings of HIV/AIDS Theory). ENDGAME illustrates this vividly with the story of Nell, a middle-aged widow who re-married and later discovered a letter from a blood bank to her husband advising him to seek medical assistance because his blood had tested “HIV-positive”. This story is featured more than once in ENDGAME, yet nowhere are two vital points made:
1. For screening in blood banks, tests for any condition are made as sensitive as possible, at the cost of lower specificity: it is essential that no infected blood be used, so false positives do not matter, it’s better to discard some perfectly good blood than to infect someone. Therefore there is a high proportion of false positives on blood-bank screening tests.
2. Specifically for HIV, all the respectable mainstream sources stress the need for confirmatory tests after an initial positive.
Yet nowhere is the point made in ENDGAME that Nell’s husband’s “positive” test should not and could not be accepted on its face as a diagnosis of infection, in absence of further testing.
Other black women are shown who had similar experiences and immediately blamed their partners for infecting them. Yet copious data show that black women are about 20 times as likely to test “HIV-positive” as white women, no matter what the reason may be — and there are dozens of possible reasons for testing “HIV-positive” that have nothing to do with a sexually transmitted retrovirus. One young lady describes her foolishness in having intercourse with an older man who had charmed her, only to fall ill within weeks of a mysterious illness that brought her to death’s door before doctors realized it was AIDS. Nell, too, relates that she felt ill already during her honeymoon. Whatever happened to the average latent period of about 10 years between infection and illness? Has there ever been an officially described case of AIDS following so soon after infection? Did “HIV” in her case collapse the immune system almost instantaneously?
Other misinformation:
There are plenty of other aspects of ENDGAME that deserve censure. A stylistic one concerns the narration. You need to listen to it yourself, because I don’t quite know how to describe it: the voice is somewhat hushed, breathless, low-pitched — one might take it as coming from a severely depressed woman; at the same time it is portentous, rather like the lead-in to the punch line of a horror story.
In terms of substance, many dangerous shibboleths are disseminated, for instance that the epidemic in the black community could have been nipped in the bud, were it not for “silence”, “stigma”, lack of testing, lack of treatment.
Many of the comments from a range of individuals indicates that illness and death in the black community are almost routinely ascribed to HIV/AIDS.
Phill Wilson tells at least a whitish lie when he describes himself as “HIV-positive” for 32 years, given that there was no HIV and no HIV tests for the first five of those years. He also insinuates that antiretroviral drugs have kept him healthy all those years. If so, he must be a very rare survivor of AZT poisoning from 1987 to 1996, when about 150,000 individuals were killed by AZT.
The fact of the matter is that no amount of testing and no amount of safe sex and no amount of pre-exposure prophylaxis will alter the relative rates at which black, white, Asian and Hispanic Americans and Native Americans test “HIV-positive”. Those rates have remained the same for a quarter of a century, because the tests are racially biased; something in the tests responds to racially correlated genetics — see the copious official data collated in The Origin, Persistence and Failings of HIV/AIDS Theory.
ENDGAME closes on a supposedly optimistic note by mentioning that the US government announced a new strategy in 2010, focusing on 12 cities most severely affected by AIDS. Washington DC leads, with “5-8%” of the adult population infected. Phill Wilson points out that if the African-American community were a country, it would rank 16th in the world for prevalence of HIV/AIDS and would qualify for assistance under the PEPFAR program.

Predicting is fraught with pitfalls, especially predicting the future, as Yogi Berra reminded us. But I make this prediction with utter confidence. Nothing will prevent blacks from testing “HIV-positive” at rates of between about 5 and about 20 (in the lower range for males and the upper ones for females). Administering prophylactic antiretroviral drugs will lead to increased rates of illness and death.
What I cannot predict is how long it will take for this genocide to become undeniably obvious.

ENDGAME is replete with well-meaning, well-intentioned, dedicated individuals spouting shibboleths that are factually wrong and whose consequences in action and in practice are bringing enormous harm to innumerable people.

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.”

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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.