On point 11, "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)? "

In other words, as someone can test negative, but still have a 'viral load' that can be
'counted', this makes AID$ $cience the only science in which you can quantify what
you cannot qualify.

Alex

http://barnesworld.blogs.com/barnes_world/2006/11/the_hivaids_hyp.html

November 21, 2006
Darin Brown Has 20 Unanswerable Questions for AIDS Inc.

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 for reply, after which it will be published 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)?

REFERENCES

============

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26. Stolberg, Sheryl Gay, "For Retired Chimps, a Life of Leisure", The New York Times, January 7,
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http://www.virusmyth.net/aids/data/pdafrica.htm

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
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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,
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33. "AIDS dissident" article at AIDS Wiki, 2006.
http://www.reviewingaids.org/awiki/index.php/AIDS_dissident, Footnote #8.

175pxdarinbrown_2 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.