The HIV/AIDS hypothesis is incompatible with reality, as demonstrated by the following twenty statements of fact (phrased in the form of questions). After twenty years and billions of dollars of research, the orthodoxy remains totally unable or unwilling to explain or even acknowledge these facts. Nevertheless, proponents of the HIV hypothesis continue to adhere to the "truthiness" of "HIV = AIDS", rather than admit to their collapsing cardboard castles.
Some of these questions have been asked in the literature since 1987, others are more recent. None has yet received a proper answer, although two web documents, from the NIH and Nature (each of which has been completely refuted, see here and here), purport to address some of them. Because of this, I added to each question what I hope is sufficient explanation to dissuade the pods of AIDS Inc. from their favorite internet ploy when similar challenges have been presented on other weblogs -- namely to quickly cobble a bunch of "refs" and "quotes" from these pieces of scientific dreck, add an adolescent comment, and pretend that the matter has been dealt with rigorously enough to satisfy a not-too-bright undergraduate, not to mention a qualified scientist. I have also asked Otis to close the comments.
However, as has been done in the past when a representative of the establishment presents one of their typical rebuttals, YBYL offers the opportunity for anyone to prepare a full response to any or all of the points above, and send it to me. It will be published, along with my reply, in full.
Lastly, the 20 Questions in the graphic are also unanswerable, but unlike the ones below, they are very funny not deeply disturbing.
1. Why have the "HIV proteins" used for antibody tests (in particular, the Western blot test) remained unchanged for 20 years (1-3), given the enormous "genetic variability/mutation rate" of HIV (4-6)?
Nearly twenty years after the advent of HIV Western blot testing, the major proteins considered to be "HIV proteins" remain as follows: p17/18, p24/25, p31/32, gp41, p53/55, gp120, and gp160 (1, 2). Yet genomic studies report 10^9 to 10^10 virions produced each day, and a mutation rate of approximately 3 x 10^-5 per nucleotide base per cycle of replication, leading to many variants of HIV in a single infected patient in the course of a single day (4). Many authors describe HIV as a "quasispecies" (4-6). It is anomalous that this "huge range of genetic configurations" (5) of "HIV quasispecies" which has developed over the past 20 years has always been detectable by antibody tests using the same core proteins, having sensitivity and specificity supposedly exceeding 99.7% (7).
2. Why has HIV prevalence had a constant asymmetrical geographic distribution over the past 20 years in the US (8)?
See the section "Unchanged Geographic Distribution" in reference (8). Bauer notes, "This fact adds to the conundrum that F(HIV) [prevalence of HIV antibodies] has not increased in magnitude since 1985: If HIV arrived around 1970 in Los Angeles, San Francisco, and New York, it would have needed to spread explosively in just a few years to produce a geographic pattern that then remained stable since 1985; and if it had indeed spread so rapidly at first, why did it then stop spreading almost immediately?" (8)
3. Why does HIV discriminate so well by race (9)? Why do organisations such as the CDC offer patently racist explanations for this data (8-10)?
In reference (8), Bauer notes, "In the overwhelming majority of reports, the ratio of F(HIV) [prevalence of HIV antibodies] to that among whites is: Asians, 0.5-0.9; Native Americans, 1.1-1.6; Hispanics, 1.5-3.0; and blacks, 2.5-6.0. One has the choice of seeking for these observations a behavioral explanation or a non-behavioral one. Any behavioral explanation raises ghosts of such longdiscarded and properly discarded theories as phrenology, physiognomy, or Cesare Lombroso's Criminal Anthropology, which asserted a strictly determinist connection between behavior and physique (or genome). Fortunately, a less racist and more scientifically (as well as politically) correct explanation is available."
The CDC offers the following behavioural explanation for this fact: "Seroprevalence was substantially higher among blacks than among whites in nearly every serosurveillance population... In the Western states, HIV seroprevalence was similar among Hispanics and whites, while in states along the Atlantic Coast, seroprevalence was higher among Hispanics than among whites. The marked racial and ethnic differences in HIV prevalence, even among persons treated in the same clinic, suggests that both behavioral norms and complex social mixing patterns within racial and ethnic groups are important determinants of HIV transmission risk." (10)
4. Why have American blacks always tested HIV-positive about 5 times as often as whites, yet the ratio of AIDS cases between blacks and whites has increased 3-fold (9)?
Since the ratio of AIDS cases between blacks and whites has increased 3-fold, if HIV is the cause of AIDS, one would expect to find the ratio of F(HIV) between blacks and whites to have increased in a similar fashion over time. This is not the case: see Table 5, "Data for HIV From the Same Sources as in Table 3, Re-ordered Chronologically and Re-averaged as Required; AIDS Ratio Changes by Factor of 3, Frequency of Positive HIV-tests [F(HIV)] Ratio Does Not Change" of reference (9).
5. Why do most individuals with low CD4 counts not develop AIDS-defining illnesses (11, 12)?
Macy & Adelman (11) reported that 5% of "a large cohort of normal healthy persons" seeking life insurance had CD4 counts below 430/mm^3, and another 5% had an inverted CD4/CD8 ratio of less then 1.00. Estimating the number of "normal healthy persons" in the US at 200,000,000, since 5% of 200,000,000 is 10,000,000, it follows that "normal healthy persons" with low CD4 counts or inverted CD4/CD8 ratio greatly outnumber, by at least a factor of 10, HIV positive individuals in the US. Therefore, the "opportunistic infections" of AIDS patients in the US cannot be due to an HIV-mediated destruction of CD4 cells.
Similarly, in a meta-analysis of CD4 counts in Africa (12), about 1.5% of HIV-negative Africans had CD4 counts below 350. (This number was obtained by estimating raw numbers from Table 1 in reference (12).) In some areas, such as Ethiopia, Guinea Bissau, and Uganda, between 3% and 5% of HIV-negative Africans had CD4 counts below 350 (12). Thus, even in Africa, where HIV prevalence is higher than in the US or Europe, there is a significant number of people with low CD4 counts which cannot be explained by HIV infection.
6. Why do "viral load", CD4 counts, and culturable virus have almost no correlation with each other (13, 14)?
Craddock (14) performed standard coefficient of determination (R^2) computations on the raw data of Piatak (13). He found the correlations between "viral load", CD4 counts, and culturable virus to be virtually nil.
7. Why did roughly half of all HIV-positive patients in a study have zero (undetectable) culturable virus and almost all of them have nearly undetectable culturable virus (13, 14)?
8. Why does "viral load" account for only 4% of the change in CD4 count cell loss in HIV-positive asymptomatics (15)?
Rodríguez et al (15) give a coefficient of determination (R^2) of just 4% between "viral load" and model-estimated CD4 cell loss rate. In an accompanying commentary, Henry et al (16) admit that "... Twenty-five years into the HIV epidemic, a complete understanding of what drives the decay of CD4 cells -- the essential event of HIV disease -- is still lacking" and "... The findings presented by Rodríguez et al provide support to those who favor nonvirological mechanisms as the predominant cause of CD4 cell loss", yet rather than interpreting the data as evidence against the HIV hypothesis, they make the following incredible rationalization: "... The second and potentially more exciting implication of the findings of Rodríguez et al is that future improvements in the treatment of HIV infection and AIDS may result from improved understanding of the 90% of CD4 cell depletion that remains enigmatic."
9. Why do 10% of control samples from blood donors test Western blot positive (17)?
10. Why do 20-40% of ELISA-negative blood donors test Western blot "indeterminate" (18)?
11. Why are very high "viral loads" found in HIV-negative individuals? (19-21) Why is it NOT nonsensical that a laboratory test which purportedly measures the "amount of virus" requires other independent (antibody) tests to determine if virus is actually present in the first place (22)?
Busch et al (19) report: "Positive results were reported with HIV-1 gag primers (SK38/39) for 48 of 188 separate PCR determinations on DNA extracts from 44 serum samples from seropositive patients (25.5% sensitivity). HIV-1 gag signal was also reported for 28 of 151 PCR determinations on 34 samples from noninfected blood donors (18.5% false-positive rate)... These results indicate that current techniques for detecting cell-free HIV-1 DNA in serum lack adequate sensitivity, specificity, and reproducibility for widespread clinical applications."
Gerberding (20) reports: "The failure to demonstrate seroconversion...among those with positive PCR tests suggests that false positives occur even under stringent test conditions. The low predicitive value of a positive or indeterminate PCR test...contraindicates the routine use of gene amplification in this clinical setting."
Schwartz et al (21) report a a person with a viral load of 100,000 who was negative on the ELISA and Western Blot antibody tests.
The Roche Amplicor test kit disclaimer (22) states: "The amplicor HIV-1 monitor test is not intended to be used as a screening test for HIV, nor as a diagnostic test to confirm the presence of HIV infection."
12. In acutely infected CEM cultures, why does cell death attributed to HIV-mediated apoptosis occur 6-7 days post-infection, while maximum virus production occurs 10-17 days post-infection (23)? The cause should always precede the effect.
13. Why do HIV test kit manufacturers now seem less convinced than ever that HIV causes AIDS (24)?
Culshaw (24) uncovered the following statements in HIV test kit disclaimers: "AIDS, AIDS-related complex and pre-AIDS are thought to be caused by HIV."; "Epidemiologic data suggest that the Acquired Immune Deficiency Syndrome (AIDS) is caused by at least two types of human immunodeficiency viruses, collectively known as HIV."; "Published data indicate a strong correlation between the acquired immune deficiency syndrome (AIDS) and a retrovirus referred to as Human Immunodeficiency Virus (HIV)." See the reference (24) for hypertext links.
14. How do CDC researchers know that detection of a certain combination of antibodies to proteins indicates infection with an exogenous retrovirus in a human, but not in a dog (25)?
Brown (25) notes: "Why, when antibodies of a dog react to certain proteins manufactured in a lab, is this interpreted as 'antibodies reacting to structural proteins of HIV' but at the same time NOT evidence that '[these] dogs are infected with HIV', yet when antibodies of a human react to exactly the same proteins, this is taken as evidence of 'HIV' infection?... The only way I can see the CDC can claim infection in one case and not the other, is if some additional validation process had been achieved in the one case and failed in the other. I'm not aware of any such process, as all such 'validation processes' that I'm aware of consist of simply testing WB against itself (reproducibility) or using some vague combination of individually unvalidated 'surrogate markers' and/or antibody tests and declaring such combination to be proof of infection."
15. Why has not a single chimpanzee, out of more than 250 successfully infected with HIV since 1984, developed AIDS? There is not one other human viral pathogen that cannot reproduce a similar disease in chimps.
Stolberg (26) reports: "Jessie and Dover [two chimpanzees at Yerkes National Primate Research Center] do not really have to be at Yerkes, but there is nowhere else for them to go. Bred for biomedical research, they are now unemployed, a result of a vast surplus of laboratory chimpanzees. They pass their days in small steel-and-concrete enclosures, playing with burlap bags and shredding old telephone books for entertainment... The surplus is an unexpected legacy of AIDS. In the early days of the epidemic, scientists theorized that the chimp would be a useful model to study the disease in people. In 1986, the health institutes began an aggressive breeding program that doubled the laboratory chimp population, only to find that although chimpanzees could contract the AIDS virus, they rarely became sick from it. That distinction makes it hard to use the animals to test [AIDS] treatments or vaccines."
16. Why is Pneumocystis carinii pneumonia not the most common AIDS-defining disease across all demographic and geographic spectra and why does it not occur at similar rates across demographic and geographic spectra, since it is a 100% ubiquitous latent human pathogen (27)?
17. Why do the in vivo and in vitro virus neutralizing antibodies that are present in easily assayable amounts in the blood of HIV infected people (28) not protect against AIDS if HIV is the culprit?
18. Why are exactly the same cells that HIV is said to kill in vivo not killed in vitro where productively infected cultures continue to produce 1000s of infectious particles per day for use in the various "AIDS tests" and are not protected by antibodies or "antiretroviral" drugs (29)?
19. Why are HIV and AIDS sexually equally distributed in Africa, while the ratio of male to female HIV-positive in the US is no more than 2:1, yet AIDS occurs in roughly 90% males (30)?
20. Why have improvements in "virological responses" ("viral load" and CD4 counts) to HAART not translated into decreased clinical progression to AIDS and death (31)? Among HAART patients, why do "grade 4 events" (serious or life-threatening events associated with drug toxicities) occur twice as often as "AIDS events" (32)?
BONUS: Why have all these questions been met with inadequate, if not nonexistent responses, and why have people who have raised these questions been called "irresponsible" and "dangerous to public health" (33)?
1. Papadopulos-Eleopulos E et al., 1993.
"Is a Positive Western Blot Proof of HIV Infection?", Bio/technology,
11, 696-707, 1993, http://www.reviewingaids.org
2. Constantine, Niel, 2006. "HIV
Antibody Assays", HIV InSite Knowledge Base Chapter, May 2006, http://hivinsite.ucsf.edu
3. United States Food and Drug
Administration, 2006. "Donor Screening Assays for Infectious Agents and
HIV Diagnostic Assays", http://www.fda.gov/cber
4. Robertson DL, Hahn BH, Sharp PM, 1995.
"Recombination in AIDS viruses". J Mol Evol. 40 (3): 249-259, 1995, http://www.ncbi.nlm.nih.gov
5. Vartanian, J.P., Meyerhans, A., Henry, M.
and Wain-Hobson, S. 1992. "High-resolution structure of an HIV-1
quasispecies: identification of novel coding sequences". AIDS 6:1095-1098,
6. Altman, John D. and Mark B. Feinberg,
2004. "HIV Escape: There and Back Again", Nat Med 10(3): 229-230,
7. Chou et al, 2005. "Screening for HIV:
A Review of the Evidence for the U.S. Preventive Services Task Force",
Annals of Internal Medicine, Volume 143 Issue 1, pp. 55-73, http://www.annals.org/cgi
8. Bauer, Henry, 2005. "Demographic
Characteristics of HIV -- I. How Did HIV Spread?", Journal of Scientific
Exploration, Vol. 19, No. 4, 567-603, 2005, http://www.reviewingaids.org
9. Bauer, Henry, 2006. "Demographic
Characteristics of HIV -- III. Why Does HIV Discriminate by Race?",
Journal of Scientific Exploration, Vol. 20, No. 2, 255-288, 2006, http://www.reviewingaids.org
10. Centers for Disease Control and Prevention, 1994. National HIV serosurveillance summary: Results through 1992. Vol. 3. Atlanta, GA: U.S. Department of Health and Human Services. HIV/NCID/11-93/036, p. 37.
11. Macy EM and Adelman DC, 1988.
"Abnormal T-cell subsets in normal persons", NEJM 319:1608-1609, http://www.ncbi.nlm.nih.gov
12. Williams, Brian, et al, 2006. "HIV
Infection, Antiretroviral Therapy, and CD4+ Cell Count Distributions in African
Populations", J Infect Dis 194; 1450-1458, http://www.journals.uchicago
13. Piatak M et al, 1993. "High levels
of HIV-1 in plasma during all stages of infection determined by competitive
PCR", Science. 1993 Dec 3;262(5139):1585-6, http://www.ncbi.nlm.nih.gov
14. Craddock, Mark. "Commentary on the
Durban Declaration Rebuttal", http://www.healtoronto.com
15. Rodríguez B et al., 2006.
"Predictive Value of Plasma HIV RNA Level on Rate of CD4 T-Cell Decline in
Untreated HIV Infection", JAMA.2006; 296: 1498-1506, http://www.ncbi.nlm.nih.gov
16. Henry WK et al., 2006. "Explaining,
predicting, and treating HIV-associated CD4 cell loss: after 25 years still a
puzzle", JAMA. 2006; 296:1523-5, http://www.ncbi.nlm.nih.gov
17. Lundberg, G.D. 1988. "Serological
Diagnosis of Human Immunodeficiency Virus Infection by Western Blot
Testing", JAMA 260:674-679, http://www.ncbi.nlm.nih.gov
18. Proffitt MR & Yen Lieberman B, 1993,
"Laboratory diagnosis of HIV infection", Infectious Disease Clinics
of North America 7(2).; 203-215, http://www.ncbi.nlm.nih.gov
19. Busch MP, Henrard DR, Hewlett IK,
Mehaffey WF, Epstein JS, Allain JP, Lee TH, Mosley JW, 1992. "Poor
sensitivity, specificity, and reproducibility of detection of HIV-1 DNA in
serum by polymerase chain reaction", The Transfusion Safety Study Group. J
Acquir Immune Defic Syndr. 1992;5(9):872-7, http://www.ncbi.nlm.nih.gov
20. Gerberding JL, 1994. "Incidence and
prevalence of HIV, hepatitis B virus, and cytomegalovirus among health care
personnell at risk for blood exposure: Final report from a longitudinal
study", J Infect Dis 170; 1410-1417, http://www.ncbi.nlm.nih.gov
21. Schwartz DH et al., 1997. "Extensive
evaluation of a seronegative participant in an HIV-1 vaccine trial as a result
of a false positive PCR", Lancet 350; 256-259, http://www.ncbi.nlm.nih.gov
22. Roche Amplicor test kit disclaimer.
23. Laurent-Crawford, A. G., Krust, B.,
Muller, S., Rivière, Y., Rey-Cuillé, M.-A., Béhet, J.-M., Montagnier, L. &
Hovanessian, A. G., 1991. "The Cytopathic Effect of HIV is Associated with
Apoptosis", Virol. 185:829-839, 1991, http://www.ncbi.nlm.nih.gov
24. Culshaw, Rebecca, 2006. "Dear Dr.
Culshaw", Hank's "You Bet Your Life", 20 October 2006, http://www.reviewingaids.org
25. Brown, Darin, 2006. "Why Owners of
Ab+ Canines Need Not Be Concerned", Hank's "You Bet Your Life",
27 September 2006, http://www.reviewingaids.org
26. Stolberg, Sheryl Gay, "For Retired Chimps, a Life of Leisure", The New York Times, January 7, 2003.
27. Pifer, L.L., 1984. "Pneumocystis
carinii: a misunderstood opportunist", Eur. J. Clin. Microbiol. 3:
28. Daar, E.S., Moudgil, T., Meyer, R.D. and
Ho, D.D., 1991. "Transient high levels of viremia in patients with primary
human immunodeficiency virus type 1 infection", New Engl. J. Med. 324:
29. Duesberg, PH, 1992. "AIDS Acquired
by Drug Consumption and Other Non-contagious Risk Factors", Pharmacology
and Therapeutics, Vol. 55: 201-277, 1992, "HIV Assumed to Kill
30. Duesberg, PH, 2000. "The African AIDS
Epidemic: New and Contagious, or Old Under a New Name?", http://www.virusmyth.net/aids
31. May, MT et al, 2006. "HIV treatment
response and prognosis in Europe and North America in the first decade of
highly active antiretroviral therapy: a collaborative analysis", Lancet.
2006 Aug 5;368(9534):427-8, http://www.ncbi.nlm.nih.gov
32. Reisler RB, et al, 2003. "Grade 4
events are as important as AIDS events in the era of HAART", J
Acquir Immune Defic Syndr. 2003 Dec 1;34(4):379-86, 33, http://www.ncbi.nlm.nih.gov
33. "AIDS dissident" article at
AIDS Wiki, 2006. http://www.reviewingaids.org
Darin C. Brown received his Ph.D. in mathematics from the University of California, Santa Barbara in 2004. His dissertation was in algebraic number theory, although he tells us he also has "interests in Fuchsian groups, category theory, and point-set topology". (Fuchsian groups? Sounds exciting !) His "mathematical lineage traces to Stark and Chebyshev". Dr. Brown is also the webmaster at the AIDS Wiki.