Top 100 AIDS Science Inconsistencies
By John Kirkham



All of the observations below can be substantiated by independent
research. How long can the HIV=AIDS=Death dogma be maintained in the face
of so many scientific cracks?

1. AIDS occurs in the absense of HIV (65, 87), a new medical definition
(Idiopathic CD4+ T-cell lymphocytopenia) was therefore created.
2. HIV does not satisfy Koch's postulates, the criteria that must be met
in order to prove that a microbe causes a disease (90)
3. Anti-HIV drugs, including protease inhibitors, destroy T-cells (4-10)
4. Septrin (also called Septra, Bactrim, Co-trimoxazole) and anti-HIV
drugs destroy mitochondria (11,12)
5. The PCP (Pneumocystis Carinii pneumonia) fungus becomes resistant to
Septrin (12)
6. Recreational drugs (heroin, poppers, crystal met, ecstasy, cocaine)
reduce CD4 cell numbers (13-18, 58, 66-68)
7. HIV positive patients recover after they stop taking drugs (58)
8. Recreational drugs cause AIDS-defining diseases (see table 7 of 58)
9. Anti-HIV drugs cause AIDS-defining diseases (58)
10. Anti-HIV drugs inhibit human enzymes (11)
11. HIV positive Africans in dire poverty in Uganda and no access to
anti-HIV drugs lived as long as HIV positives in the West who took
anti-HIV drugs (33)
12. There are no comparative studies of survival in HIV negatives and
combo-free HIV positive heterosexuals with no other risk factors.
13. Only 38% of healthy long-term positives had ever used AZT or other
nuleoside analogs compared with 94% of progressors (80)
14. Decreases in AIDS cases preceded the introduction of new drug
treatments (Dec 1995) by three full years (see fig. 6 of 106)
15. Anti-HIV drugs have anti-microbial effects (49, 50, 10)
16. The introduction of AZT did not cause a decline in the AIDS death rate
(105)
17. In the only long term trial of AZT (The Concorde study) 172
participants died, 169 while taking AZT, 3 while on placebo (51)
18. Nucleoside analog drugs suppress/destroy the bone marrow where all
immune system cells are born (26, 32, 111)
19. HIV+ children born to AZT treated mothers had a higher probability of
developing severe disease or severe immunsuppression (53)
20. "Drug holidays" recover immune responses
21. AZT caused the same transient increase in CD4 count in HIV negatives
as in HIV positives (55)
22. There are no controlled studies showing that AIDS occurs in the
absense of all other possible non-HIV causal factors.
23. Long-living, healthy, drug-free HIV positives are mostly ignored by
AIDS researchers
24. Apart from the early (fraudulent) AZT studies and the Concorde study
no efficacy studies compare drugs with placebo
25. There are well documented, non-HIV causes for every AIDS disease
26. The incidence of AIDS-defining diseases among Western non-drug users
has not been shown to exceed national backgrounds (58)
27. Early AIDS coincided with the cumulative effects of unprecedented,
intense use of volatile nitrite (poppers) as a aphrodisiac marketed almost
exclusively to homosexuals (102)
28. AIDS can be treated effectively without anti-HIV drugs (39-42, 112)
29. On average viral load overestimates infectious HIV by a factor of
60,000 (21)
30. Even a PCR method that can detect 1 infected cell in 100000 found very
little HIV DNA in HIV positives (23)
31. HIV could not be cultured from people with a detectable viral load
(19, 21)
32. HIV has never been properly isolated (20)
33. After many billions of dollars of research effort over 20 years, HIV
scientists still cannot explain how HIV causes AIDS.
34. After many billions of dollars of research effort over 20 years there
is no vaccine and no cure, there are only toxic drugs
35. There was no increase in HIV seroprevalence outside risk groups in the
UK despite record STD rates and teenage pregnancy rates (25)
36. HIV DNA was found to be constant from the time of seroconversion but
CD4 count continually went down (29)
37. CD4 count goes down and viral load goes up while on the anti-HIV
drugs.
38. AZT is hardly triphosphorylated by the body so it cannot possibly have
an anti-HIV effect (30)
39. AZT has no effect on HIV DNA but makes viral load (HIV RNA) go down
(31)
40. Research throughout the 1970s showed that retroviruses do not kill
cells.
41. The probability of heterosexual transmission of HIV was found to be
very low (1 in a 1000 for male to female and 8 times less likely for
female to male) (34)
42. HIV antibody tests can give repeated false positives and
seroreversions can occur (95-100, 114-116)
43. HIV tests are sensitive to non-specific antibody binding
44. HIV tests involve an arbitrary dilution factor, everyone tests
positive (because of non-specific antibody binding) if their serum is
undiluted (104)
45. All the proteins used in the HIV test are associated with retroviral
genes that are found naturally (endogenous) in all humans (72)
46. Endogenous retroviruses can generate immune responses in humans (73,
74)
47. None of the HIV proteins tested for have been proven to belong to HIV
(75)
48. There are over 60 different conditions, including pregnancy, that have
been known to generate false positives on the HIV test (91)
49. The Elisa, Western Blot and PCR tests for HIV all carry disclaimers
nullifying their detection of HIV
50. The criteria for HIV-positivity used in the antibody tests varies
between countries and between organisations within a country and can
produce indeterminate (neither positive or negative) results (75, 109) The
Western Blot HIV test, widely regarded as the most accurate, is not used
in England and Wales because it is regarded as inaccurate.
51. The viral load PCR primers were found to be non-specific for "HIV"
genetic sequences (35)
52. The viral load test gives false negatives (36)
53. The viral load test gives false positives (36, 113)
54. The viral load test has low reproducibility (36-38)
55. Direct measurements showed no correlation between viral load and CD4
count (43)
56. Many conditions cause reduced CD4 counts (86)
57. CD4 counts between 200 and 300 have been observed in healthy HIV
negatives (87)
58. There are no studies comparing CD4 cell variations in combo-free HIV
positives (with no risk factors) and HIV negatives.
59. According to the AIDS establishment, a heterosexual AIDS "epidemic" of
African origin started off in the West as a homosexual "epidemic"
60. In 1985 HIV incidence in Southern Africa was confined to homosexuals
who had been to the US and those who had had sex with them (88, 89).
61. The USA was found to be the world's most sexually promiscuous nation
(27)
62. Condoms (made from polyisoprene) have holes in much larger than HIV
(28, 110)
63. Reducing STD incidence in Africa did not reduce the rate of HIV
seroconversion* (101)
64. Only a minute proportion of Africans have actually been tested for
HIV, seroprevalence estimates are derived from extrapolations based on
unrepresentative samples from maternity clinics.
65. In Africa a single positive ELISA test or even a single "rapid"
(saliva/urine) test is considered proof of HIV infection, "proof" in the
developed world requires a series of tests
66. HIV seroprevalence was found to be much lower in South African prisons
than in the general population (1)
67. The vast majority of African "AIDS patients" tested HIV negative (44,
45)
68. In "AIDS ravaged" Zambia since 1980 the population has increased and
even the rate of increase in population has increased! (46)
69. In "AIDS ravaged" South Africa many coffin makers are either doing a
slack trade or have gone out of business (47)
70. The total number of AIDS cases in Africa consists almost entirely of
estimated cases rather than known, registered cases (54)
71. PCP is the typical AIDS defining disease in Western adults but it is
almost entirely confined to young children in Africa (2,3)
72. There is no Western heterosexual AIDS epidemic
73. IVDUs who consistently used a clean needle exchange program were 10.2
to 22.9 times MORE likely to test HIV positive than non-users (48)
74. Non-human primates "progress" to AIDS (SAIDS) much quicker than humans
do (107)
75. SIV does not cause SAIDS in wild primate populations (108)
76. SIV seroprevalence is too low in wild primate populations to account
for SIV resistance in these populations (22)
77. SIV seroprevalence in captive SIV naÔve primate populations was found
to be very low (22)
78. Until the early 1930s many thousands of European men received
transplants from chimpanzees and did not get AIDS (62)
79. Uganda study showed HIV-positivity did not indicate a new cause of
disease, only decreased mortality in HIV negatives (52)
80. One thousand medical staff a year accidentally contract hepatitis from
needles yet by 1998 there were no documented cases of surgeons or
emergency medical technicians/paramedics getting AIDS, or even HIV, from
occupational exposure (58, Table 16 of 106)
81. All AIDS patients have lowered levels of glutathione, the major water
soluble intracellular antioxidant (59, 60)
82. The antioxidant N-acetyl cysteine inhibits "HIV replication" (61)
83. Reactive oxygen species are implicated in the induction of HIV
expression and cell death (40)
84. Treatment with oxidising, mitogenic*** agents is necessary for HIV
"isolation" from cell culture (56, 57)
85. Significant HIV replication was found to follow rather than precede
AIDS defining disease (94)
86. Low T-cell counts were shown to occur before HIV seroconversion and to
predict seroconversion (92, 93)
87. HIV-like genetic sequences have been found in the HIV negative human
genome (63)
88. Epitopes** of HIV regulatory proteins tat, rev and nef are expressed
in normal human tissue (71, 116)
89. Toxic intracellular stresses can create novel genetic sequences (64)
90. HIV showed over 40% variation in an essential gene (protease) sequence
within a single subtype (103)
91. Foreign protein transfusions were found to be immune suppressive (79,
81, 84, 85)
92. Hemophiliacs can have hypergammaglobulinaemia which can cause false
HIV positive test results (69)
93. Up to 99.9% of HIV genomes in plasma may be defective (70)
94. Mortality in hemophiliacs began to increase in exactly the same year
they began taking AZT (81, 82)
95. The AIDS risk of hemophiliacs on AZT was 4.5 times higher, and
mortality 2.4 times higher, than untreated controls (83)
96. Infectious HIV (a delicate virus) does not survive the Factor VIII
preparation process (76-78)
97. HIV theorists have made incorrect predictions throughout the HIV era.
98. Corticosteroids and endogenous cortisol suppress cellular immune
responses and cortisol destroys immature T-cells (24)
99. Effective cellular immunity relies upon nitric oxide gas defence, see
for example Eur. J. Immunol. 2002, 32(5):1455-63
100. AIDS spreads non-exponentially, unlike infectious disease (58)

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Footnotes

*Conversion from HIV negative to HIV positive
**Epitopes are part of a molecule against which antibodies are made
***Stimulates cell division

On Sun, 04 Apr 2004 20:45:46 -0400, "PaulKing"
<aimulti@aimultimedia.com> wrote:

When and where was this published? Indeed, many of these are not in
the slightest "inconsistencies."

THAT dogma should die. LIFE eventually leads us all to death. But HIV
need not be a death sentence.

This is not an inconsistency. Lung disease can occur in the absence of
mycobacteria infection. Does it mean TB doesn't cause lung disease in
many productively infected individuals?

This has been refuted many times. See:
http://www.sfaf.org/treatment/beta/b...iv_causes.html
http://www.niaid.nih.gov/publications/hivaids/12.htm

This is a disingenous statement. Indeed, taking the most recent
citation, one can see that the article discusses how HIV induces CD4+
cells to undergo apoptosis (cell suicide) and this may be PREVENTED by
using some antivirals, including protease inhibitors. But they ALSO
show that higher concentrations of protease inhibitors may cause
damage. There is no question that the ARV therapies have side effects
and toxicities! Some of these may be managed (and protecting
mitochondria seems EXTREMELY important, especially via reducing
excessive oxidative stress using antioxidants).

Here is the paper' s abstract::
Estaquier J, Lelievre JD, Petit F, Brunner T, Moutouh-De Parseval L,
Richman DD, Ameisen JC, Corbeil J. Effects of antiretroviral drugs on
human immunodeficiency virus type 1-induced CD4(+) T-cell death. J
Virol. 2002 Jun;76(12):5966-73.

EMI-U 9922 INSERM/Universite Paris 7, IFR02, AP-HP, Hopital
Bichat-Claude Bernard, Paris, France. jestaqui@pasteur.fr

Apoptosis of peripheral blood T cells plays an important role in the
pathogenesis of human immunodeficiency virus (HIV) infection. In this
study, we found that HIV type 1 (HIV-1) primes CD4(+) T cells from
healthy donors for apoptosis, which occurs after CD95 ligation or
CD3-T-cell receptor (TCR) stimulation. CD95-mediated death did not
depend on CD4 T-cell infection, since it occurred in the presence of
the reverse transcriptase inhibitor didanosine (ddI). In contrast,
apoptosis induced by productive infection (CD3-TCR stimulation) is
prevented by both CD95 decoy receptor and ddI. Our data suggest that
HIV-1 triggers at least two distinct death pathways: a CD95-dependent
pathway that does not require viral replication and a viral
replication-mediated cell death independent of the CD95 pathway.
Further experiments indicated that saquinavir, a protease inhibitor,
at a 0.2 microM concentration, decreased HIV-mediated CD95 expression
and thus cell death, which is independent of its role in inhibiting
viral replication. However, treatment of peripheral blood mononuclear
cells from healthy donors with a higher concentration (10 microM) of
an HIV protease inhibitor, saquinavir or indinavir, induced both a
loss in mitochondrial membrane potential (DeltaPsim) and cell death.
Thus, protease inhibitors have the potential for both beneficial and
detrimental effects on CD4(+) T cells independent of their
antiretroviral effects.


Yes, they can. And some people are more susceptible to these side
effects than others.


Yes--as can any drug result in pathogens developing resistance.

However, this is NOT an inconsistency in terms of the reality of HIV
or its effect on immune, endocrine and neurological function.

Yes--but in ALL cases, CD4 counts can recover once the drugs are
withdrawn (people stop taking them). Review those data.

However, this is NOT an inconsistency in terms of the reality of HIV
or its effect on immune, endocrine and neurological function.

Recover what? This is dangerously stupid comment. The cite refers to a
paper: Genetica 1998, 104:85-132 by Duesberg and Rasnick. Hardly a
reliable source. Duesberg insists all AIDS patients are drug users.
Well, this is stupid. What he does NOT recognize is that his loose
definition of drug user encompasses a LOT more people. MANY people who
are not gay or male are drug users, yet we do not see AIDS in
them--unless they have HIV. Women. Straight. Lesbian. Any ethnicity in
the U.S.

LOL. Drugs don't cause diseases! But yep, they can increase
susceptibility to diseases. Depends a LOT on the drug--and how it is
used. Whether it is Xanax or alcohol or crack or heroin or ibuprofen.

However, this is NOT an inconsistency in terms of the reality of HIV
or its effect on immune, endocrine and neurological function.

More reliance on Duesberg. Will get back to this...but even if it is
true: this is NOT an inconsistency in terms of the reality of HIV or
its effect on immune, endocrine and neurological function.

In some sense it can be--i.e., HIV may cause neuropathy. So can d4T
and ddI. But they won't cause CD4 counts to deplete. AZT can cause
anemia! Yep! But people generally recover if the drug is stopped.
Anemia is not AIDS.

Grapefruit juice inhibits human enzymes.

However, this is NOT an inconsistency in terms of the reality of HIV
or its effect on immune, endocrine and neurological function.

Not all Africans are living in dire poverty. Many of the people dying
of AIDS are truck drivers, sex workers, teachers, physicians, military
personnel, preachers, nurses, wives, children. Poverty certainly makes
living with HIV MUCH WORSE. AND IT MUST BE ADDRESSED!!

However, this is NOT an inconsistency in terms of the reality of HIV
or its effect on immune, endocrine and neurological function.

This sounds like a really bone headed trial design with the ethics of
a Mengele underlying it.

However, this is NOT an inconsistency in terms of the reality of HIV
or its effect on immune, endocrine and neurological function.

This citation is from 1994 and is thus of dubious value. But it is
also incredibly disingenuous. Long-term healthy positives (i.e., high
CD4 counts) do not NEED to use AZT or any other medication.

This is an interesting observation which I think makes a disingenuous
use of statistics. I would like to see others thoughts on this. My
thought too is that many people I knew who were about to die,
literally, got into drug trials (that is, before approval) or expanded
access and survived.

This is NOT an inconsistency in terms of the reality of HIV or its
effect on immune, endocrine and neurological function.


No surprise. As a monotherapy, the drug sucked. And they overdosed
people on it at 1200 mg. Indeed, I'd say the current 600 mg is too
much. Ann Collier's work suggests 300 mg may work as well. In the
context of combination therapy, tho, the same citation shows a
dramatic drop off in death rate. See:
http://www.cdc.gov/hiv/stats/hasrsupp81/fig9.htm

OK--stopping here for now. I think this is inaccurate. Concorde did
show that early AZT use wasn't very effective. Surprise. However, it
did NOT have this as a major finding.

Will get back to more in a bit. But so far, this list of items is
pretty lame. And if you're going to be your life on this to justify
ignoring HIV disease--well, you will probably die believing this
ignorant codswallop.

George M. Carter

You (Paul King, AIDS DissiDUNCE) already posted this same message
here, are you forgetful or inconciderate? Why must you over post, it
makes you look like a finatic, a crazed lunatic. At least you show
yourself in your true colors, a spamming liar... Every message these
person posts is done many times in the same group of messages, they
don't want you to read the real truth, so they drown out all logical
postings with their madness. I would probably go to jail for doing
this if I did it!

AIDS apologists are those who know HIV leads to AIDS (proven by
science, so much scientific proof) and we are defending the
scientifically known fact that viral pathogenesis and progression of
'HIV to AIDS' causes the eventual need for combination therapies to
prolong life. Mixed "AIDS Apologist" links here or find comments here
from both sides (dissidents and the scientific community), but still
about AIDS Apologist activities...

AIDS dissidents (better known as AIDS Denialists who are AIDS
dissidence, dissidence is anti-establishment like, against science and
progression, argumentative) deny HIV causes AIDS and claim the
medications kill the patients (AZT "over use" alone started this myth
in the late 80s, but medicine combo/therapies are working today in the
year 2000+). Basically a group of non doctors and non scientists who
challenge the conventional HIV/AIDS model or hypothesis and do not
accept the proven evidence. These dissident groups seem almost
fanatical by them posting the same message multiple times to a
targeted list of internet websites (non dissident sites of course,
clogging up the normal flow of reading material with intentions of
shutting the sites down) and insulting/bashing anyone who may not
agree.

http://www.medchecker.com/dissident/aids-dissidents.htm
http://www.medchecker.com/dissident/ (both same page)

In article <b8d83a5.0404050724.10755c60@posting.google.com> ,
http://www.HIVsearch.com <dave@poz.ca> wrote:
Inconsiderate. Evidence is, Paul King is moving in to fill the
asshole-power vacuum David Pasquarelli left behind.

You've posted this here before. PKB.

I'd never heard the term "AIDS apologist" until I heard it from you.

Apologetics is a combination of bent logic, twisted interpretation,
appeals to authority and arguments from intimidation used by the
religious to reconcile the contradictions within their belief systems
and make nonsense sound meaningful and important. (My version
of Steven J. Gould's concept of the "non-overlapping magisteria"
of science and religion is this: Science explains the evidence;
Religion explains the absence of evidence.)

The use of the term "AIDS apologist" is a disservice to the people
you denote by that term. Which side are you on, really?

--
David Canzi She couldn't get over the skimpiness of his worldly goods.
"Maybe you ought to rethink crime as a career path," she said.
"I do, all the time," he said, "but nothing else gives me the
same job satisfaction." -- Donald E. Westlake, Put A Lid On It

On Sun, 04 Apr 2004 20:45:46 -0400, "PaulKing"
<aimulti@aimultimedia.com> wrote:


This is a completely inaccurate statement regarding this study. The
design had people either on Immediate treatment or Deferred (until the
development of AIDS). What it showed, essentially (which was no
surprise to many of us at the time) was that early use of monotherapy
AZT wasn't worth squat. There was a slightly worse (but not
statistically significant) outcome for AZT users due to its toxicity.

This only underscores that starting ARV too early is not a good idea.
However, it does not mean that ARV is never a good idea. Nor does it
mean HIV doesn't cause AIDS.

See, e.g.: http://yarchive.net/med/concorde_study.html

They can. The clinical manifestations are usually neutropenia or
anemia. NOT a specific, significant decline in CD4 count. The
conditions are usually reversed once the drugs are discontinued or if
the dosage is reduced.

The numbers are rather small, however the data point to a potential
problem when AZT does not stop vertical transmission. It also appears
that these women had been treated at full dose. By contrast, other
data show that use of ARV among pregnant women that result in
prevention of transmission to the infant result in no long term
problems for the kids. Further, the rate of transmission is cut by use
of a single dose of nevirapine--though there are some serious liver
toxicities that pregnant women need to be aware of.

Other data have shown that the use of a multivitamin can further
enhance outcomes (including higher birthweight babies). See, e.g.,
Trans R Soc Trop Med Hyg. 2003 Jan-Feb;97(1):22-4. The work of Fawzie
in this regard has been stellar.

As with many other points on this list, this is NOT an inconsistency
in terms of the reality of HIV or its effect on immune, endocrine and
neurological function.

These data are in some dispute. No citation is provided. While there
can be some recovery in some immune responses (e.g., DTH), this is not
consistent in everyone by any stretch. And, unfortunately, the
deterioraton of CD4 count begins anew, in the case of people stopping
drugs with higher CD4 counts.

Again, this is NOT an inconsistency in terms of the reality of HIV or
its effect on immune, endocrine and neurological function.

This is a letter: CD4+ lymphocyte count variations in HIV-negative
subjects treated with zidovudine [letter]. No comment as I have not
read it.

This is not an inconsistency: it is inchoate babbling. What exactly
would be the design of such a study?

This is simply untrue. Various groups have been doing a great deal of
study on long-term survivors/non- or slow progressors, as well as
among cohorts of individuals who are repeatedly exposed but remain
uninfected. Clearly, this reflects a profound ignorance of the
literature.

Once effective treatments have been found that prevent death, giving a
placebo is considered unethical. Clinical trials are hard enough to
enroll, but such a study design for HIV+ people using placebo would
not enroll at all.

Yes. Utterly irrelevant to the fact that HIV causes AIDS and results
in greatly increased susceptibility to these diseases.

For example, CMV. Yes, people post-transplant on immune suppressive
therapy get CMV. But why does an otherwise healthy individual? (The
answer is NOT because he spent a couple weeks in jail.) Because the
individual is not "otherwise healthy" but rather is HIV infected and
their CD4 count has dropped below 50.

Other diseases like TB and cryptococcal meningitis do indeed occur
among immune intact people. But among people with HIV, the outcome is
more dire.

Duesberg's incoherent tripe again.

Another reputable citation. The "poppers" connection has been soundly
refuted. Sure, they're bad for you. But I knew too many people
personally who did NOT use them who got AIDS and died from HIV. I also
knew many people who DID use them and did not develop AIDS because
they did not have HIV. The problem with poppers is that they can
reduce inhibitions (and reduce condom use), increasing the chance of
being HIV infected, as well as reducing immune function, enhancing the
potential for being infected (see Am J Epidemiol. 1995 Oct
15;142(8):875-83 and Focus. 1999 Mar;14(4):5-6). Alcohol and
methamphetamine use may also have this effect. See also Prev Med. 1995
Jan;24(1):90-5.

There are other data I can draw upon. Clearly, recreational drug use
is something that needs to be addressed. "Just say No" is moronic.
Putting people in jail is inhumane, ineffective and an outrageous
waste of public resources.

Why is this point 28? Shouldn't it be point ONE?? Well....except if
the cited data do not support the bold statement. Let's see:

This is Herzenberg LA, De Rosa SC, Dubs JG, Roederer M, Anderson MT,
Ela SW, Deresinski SC, Herzenberg LA. Glutathione deficiency is
associated with impaired survival in HIV disease.

Yes, glutathione deficiency is an important piece. NAC, whey proteins
and alpha lipoic acid I think are all VERY important adjunctive
therapies. I use them to treat my HCV infection. However, I don't
think from all I have seen from MANY people that they are 100%
effective, unfortunately.

Greenspan HC. The role of reactive oxygen species, antioxidants and
phytopharmaceuticals in human immunodeficiency virus activity. (PS:
it's Medical Hypotheses.)

Again, oxidative stress. Important but not the whole issue.

Sigh. Howard was a friend of mine and I dearly miss him. This is still
an important article for people to read. But it also is NOT
inconsistent with the observation that HIV causes AIDS. Partly through
disruption of cellular redox status. For example, the interference of
the HIV tat protein with MnSOD (manganese superoxide dismutase).

This is entitled Successful treatment of lethal protozoal infections
with the ornithine decarboxylase inhibitor,
alpha-difluoromethylornithine. Ah. Love to read it. No abstract and
not sure what relevance this has.


Another misuse of cites: Inhibition of cyclooxygenase: a novel
approach to cancer prevention.

AIDS is not the same as cancer. There may be a role for COX-2
inhibitors in HIV disease.

Again, this isn't an inconsistency nor does it mean HIV does not exist
or does not cause AIDS.

Sigh. Some interesting stuff is embedded in a great deal of nonsense.
Free radical generation and disease is clearly a part of the problem.
But to conflate the myriad diseases associated with free radicals is
just idiotic. Rheumatoid arthritis, Parkinson's disease, AIDS and
cancer all have problems with redox imbalances, but they are
clinically distinct with varying etiologies. Indeed, antioxidant
therapy can help. It does NOT represent a cure nor a 100% effective
treatment that no other treatment is ever needed.

Finally, the list of things to do is just a pathetic hodgepodge of
this and that--lists with no particular nuance as to what to use, when
to use, how to use. The botanicals listed cannot just be thrown
together higglety-pigglety and have one expect resullts.

I find it funny that he also notes that "conventional" treatments
(citing works like Bartlett) may be used to treat OIs (see section
6.1). Gee.


Citation is Science 1993, 259:1749-1754 which is entitled Piatak, M.
Jr. et al. High levels of HIV-1 in plasma during all stages of
infection determined by competitive PCR. Science 259, 1749-1754
(1993).

The technology has improved in the last 11 years. In addition, this is
a disingenuous misinterpretation of the cited data as they were
comparing this technology to a less sensitive test. Abstract:

Quantitative competitive polymerase chain reaction (QC-PCR) methods
were used to quantify virion-associated human immunodeficiency virus
type-1 (HIV-1) RNA in plasma from 66 patients with Centers for Disease
Control stage I to IVC1 infection. HIV-1 RNA, ranging from 100 to
nearly 22,000,000 copies per milliliter of plasma (corresponding to 50
to 11,000,000 virions per milliliter), was readily quantified in all
subjects, was significantly associated with disease stage and CD4+ T
cell counts, and decreased by as much as 235-fold with resolution of
primary infection or institution of antiretroviral therapy. Plasma
virus levels determined by QC-PCR correlated with, but exceeded by an
average of 60,000-fold, virus titers measured by endpoint dilution
culture. Quantitation of HIV-1 in plasma by QC-PCR may be useful in
assessing the efficacy of antiretroviral agents, especially in early
stage disease when conventional viral markers are often negative.

Again, J Virol 1990, 64: 864-872 is old news. Indeed, they are looking
at proviral levels in monocytes (where they find them) and hypothesize
HIV-RNA is transcriptionally inactive in many lymphocytes...this is
indeed what has subsequently been discovered.


Culture is a weak tool. Cite 21 is discussed above (claim 29).
Cite 19: NEJM 1995, 332:201-208
The funny thing about this is that it is just a FIRST example that
refutes claim 23: the title is "Studies in Subjects with Long-Term
Nonprogressive Human Immunodeficiency Virus Infection"

Further, this statement is yet another disingenuous cherry-picking.
The authors note: "HIV could not be isolated from the plasma of the
former, who also had significantly higher titers of neutralizing
antibodies than the latter. There was viral replication, however, in
the subjects with nonprogressive infection, and virus was consistently
cultured from mononuclear cells from the lymph nodes."

Sigh. You guys really are fucking liars.

Oh horseshit. Even Peter DUESBERG says it has. Herein lies the schism
within the denialist community...some idiots say it hasn't been
isolated, others say it has. The idiots that say it hasn't have always
burbled about a "gold standard" of isolation...and give a cite of work
done by Francoise Barre-Sinoussi. The woman who discovered LAV in Luc
Montaignier's lab!!! (Later called HIV...yes, a woman discovered HIV).
Virol. 1997, 230:125-133

Anyway--not sure what this cite is yet but it led me to:
http://www.hiv.lanl.gov/content/hiv-...Gelderblom.pdf
interesting paper...

Completely irrelevant. We don't know how MOST pathogens cause disease.
Yes, we have some good descriptions, some great detail about many
aspects of many diseases (including HIV) but not yet the whole story.
Biology is complex, to put it mildly.

Point 33 is a throwaway comment that has no intrinsic value.

True for many diseases. Irrelevant to the reality, as with point 33,
that HIV exists and causes AIDS. As much as it is to the statement
that syphilis spirochetes exist and cause syphilis.

Hurray! but guardedly. Let's hope that HIV incidence among populations
declines globally.

You might note that this point is an argument AGAINST your screed.
Ther is also no increased prevalence of AIDS outside risk groups.
Hmmmm...maybe that's because the risk is from HIV.

This is not inconsistent with HIV causing AIDS and is again a
disingenuous misinterpretation of cited data. Again: J. AIDS 1994,
7:381-388 describes something different from what is stated here:

Lee TH, Sheppard HW, Reis M, Dondero D, Osmond D, Busch MP.
Circulating HIV-1-infected cell burden from seroconversion to AIDS:
importance of postseroconversion viral load on disease course. J
Acquir Immune Defic Syndr. 1994 Apr;7(4):381-8.

Irwin Memorial Blood Centers, San Francisco, CA 94118-4496.

The purpose of this study was to characterize quantitative changes in
circulating infected cells over the natural history of human
immunodeficiency virus (HIV) disease in relation to
clinical/immunological outcome. HIV-1 gag DNA polymerase chain
reaction (PCR) and peripheral blood mononuclear cell (PBMC)
co-cultures were performed on limiting dilutions of cryopreserved PBMC
from specimens collected at enrollment and after 5 years of follow-up
from nine seropositive subjects classified as rapid progressors, nine
intermediate progressors, and 10 nonprogressors. Limiting dilution PCR
was also performed on serial pre/postseroconversion specimens from 18
seroconvertors. By quantitative DNA PCR analysis, the infected cell
burden was significantly higher at enrollment in the RP [mean of 330
PCR units (PCRU)/10(6) PBMCs] than in the IP (160 PCRU/10(6) PBMCs)
and NP (73 PCRU/10(6) PBMCs) groups (p = 0.05). When results were
analyzed on an individual level with proportional hazard regression,
baseline PCRU (p = 0.05) and CD4 slope (p = 0.0007) were significantly
associated with developing acquired immune deficiency syndrome (AIDS)
in 5 years, but baseline tissue culture infectious units (TCIU) was
not. The increase in PCR-positive cells after 5 years was modest in
all three groups (two- to fivefold), whereas the proportion of
PCR-positive cells that yielded virus in culture increased
significantly (21- to 31-fold) over time in all three groups. Infected
cell burden in postseroconversion specimens was relatively stable
within each subject, but varied greatly (from 1.6 to 1,024 PCRU/10(6)
PBMCs) among subjects.


No citation for this bit of delirium. Actually, such discordant
results CAN happen. I know one guy that has seen this. But in general,
this is not the case: CD4 goes up and HIV load down with ARV is the
general rule and I have seen it time and time and time again.

Enough for today! Over a third of the way through the list and it
looks to be a big, messy crock of bullshit.

George M. Carter

On Sun, 04 Apr 2004 20:45:46 -0400, "PaulKing"
<aimulti@aimultimedia.com> wrote:

Man...if these are the top 100...pretty lame. Here we go for some
more.

Now to me, the sad thing about this list is that there are SO many
important questions regarding HOW HIV causes AIDS. Answers to these
can lead to better understanding of the disease and thus, more areas
for intervention.

Well, that's stupid. Cite is Current Medical Research and Opinion
1999, Vol. 15, supplement 1. No page numbers are provided and a review
on Medline does not indicate any article titles relevant to the
comment.

In any case, triphosphorylation of AZT is what permits it utilization
by the RNA uptake machinery and hence blocking RNA transcription. The
azide group basically truncates further RNA production. Great when it
is affecting HIV RNA. And generally not a problem with nuclear DNA
(despite Lauritsen's screechings to the contrary)...the problem and
toxicity arises when it damages mitochondrial DNA.

But it doesn't mean HIV doesn't exist or doesn't cause AIDS. So a
mis-statement to begin with and irrelevant to its intent of declaring
some kind of discrepancy.

Oh--more on this:
http://www.hiv.lanl.gov/content/hiv-...rtI/Shafer.pdf
The nucleoside RT inhibitors (NRTIs) are prodrugs that are
triphosphorylated by host cellular enzymes. The triphosphorylated
NRTIs then compete with natural deoxynucleoside triphosphates (dNTPs)
for incorporation into the newly synthesized DNA chains where they
cause chain termination. There are two biochemical mechanisms of NRTI
drug resistance. The first mechanism is mediated by mutations that
allow the RT enzyme to discriminate against NRTI during synthesis,
thereby preventing their addition to the primer DNA chain (Larder and
Stammers, 1999; Sarafianos et al., 1999a; Sarafianos et al., 1999b;
Huang et al., 1998). The second mechanism is mediated by mutations in
RT that increase the rate of hydrolytic removal of the chain
terminating NRTI and enable continued DNA synthesis (Arion et al.,
1998; Arion et al., 2000; Boyer et al., 2001; Meyer et al., 1999;
Meyer et al., 1998).


Duh. This is completely contradicting yourself dear. Implicit in this
comment is a recognition at least that HIV exists.

Reverse transcriptase happens BEFORE incorporation of new HIV DNA into
the host cells. So one would not EXPECT DNA levels to drop. But yes,
RNA levels go down. Problem is, resistance develops when it is used on
its own. And toxicities increase with dose.

LOL...this is stupid. This is 2004. Tell this to goats with CAEV, cats
with FIV and FELV, cows with Visna maedi, horses with the equine
retrovirus...etc., etc. Cytopathicity has been demonstrated for HIV;
it depends on the cell line used and the strain of virus. However,
direct cytopathicity is not necessarily the primary mechanism for the
development of AIDS!

This may be true but somehow I think it is a bit silly. If a man has a
high viral load, the sex is vigorous, the woman is nutritionally
suppressed or has been drinking, etc., the chances of her becoming
infected are higher.

But this is really completely irrelevant as a point of "inconsistency"
in terms of recognizing HIV exists or causes AIDS.

Points 42-45 above all refer to testing of HIV. These points have been
addressed in an elegant rebuttal found at:
http://www.aids.org/atn/a-375-04.html
http://www.wsws.org/articles/2000/au...aids-a26.shtml

HERVs do not cause a steady, chronic depletion of CD4 cells.

(73) Immunological Reviews 1996, 152:193-236
Intersting article, but it does not support your point. It suggests
that these endogenous retroviruses may cause autoimmune disorders in
some individuals. They are not AIDS. Nor does the article preclude or
argue against the existence of HIV or its role in the development of
AIDS. And indeed, in an not so surprising act of cognitive dissonance,
this is in direct contradiction to your statement 40 above! Here,
retroviruses ARE causing disease.

Abstract below:
Nakagawa K, Harrison LC. The potential roles of endogenous
retroviruses in autoimmunity. Immunol Rev. 1996 Aug;152:193-236.

Burnet Clinical Research Unit, Walter and Eliza Hall Institute of
Medical Research, Royal Melbourne Hospital, Parkville, Australia.

Endogenous retroviruses (ERVs) are estimated to comprise up to 1% of
human DNA. While the genome of many ERVs is interrupted by termination
codons, deletions or frame shift mutations, some ERVs are
transcriptionally active and recent studies reveal protein expression
or particle formation by human ERVs. ERVs have been implicated as
aetiological agents of autoimmune disease, because of their structural
and sequence similarities to exogenous retroviruses associated with
immune dysregulation and their tissue-specific or
differentiation-dependent expression. In fact, retrovirus-like
particles distinct from those of known exogenous retroviruses and
immune responses to ERV proteins have been observed in autoimmune
disease. Quantitatively or structurally aberrant expression of
normally cryptic ERVs, induced by environmental or endogenous factors,
could initiate autoimmunity through direct or indirect mechanisms.
ERVs may lead to immune dysregulation as insertional mutagens or
cis-regulatory elements of cellular genes involved in immune function.
ERVs may also encode elements like tax in human T-lymphotrophic virus
type I (HTLV-I) or tat in human immunodeficiency virus-I (HIV-I) that
are capable of transactivating cellular genes. More directly, human
ERV gene products themselves may be immunologically active, by analogy
with the superantigen activity in the long terminal repeat (LTR) of
mouse mammary tumour viruses (MMTV) and the non-specific
immunosuppressive activity in mammalian type C retrovirus env protein.
Alternatively, increased expression of an ERV protein, or expression
of a novel ERV protein not expressed in the thymus during acquisition
of immune tolerance, may lead to its perception as a neoantigen.
Paraneoplastic syndromes raise the possibility that novel ERV-encoded
epitopes expressed by a tumour elicit immunity to cross-reactive
epitopes in normal tissues. Recombination events between different but
related ERVs, to whose products the host is immunologically tolerant,
may also generate new antigenic determinants. Frequently reported
humoral immunity to exogenous retrovirus proteins in autoimmune
disease could be elicited by cross-reactive ERV proteins. A review of
the evidence implicating ERVs in immune dysfunction leads to the
conclusion that direct molecular studies are likely to establish a
pathogenic role for ERVs in autoimmune disease.

***
RE the other cite, same comments apply:
(74) Lower R, Lower J, Kurth R. The viruses in all of us:
characteristics and biological significance of human endogenous
retrovirus sequences. Proc. Natl. Acad. Sci. USA 1996, 93:5177-5184.

Paul-Ehrlich-Institut, Langen, Germany.

Human endogenous retroviruses (HERVs) are very likely footprints of
ancient germ-cell infections. HERV sequences encompass about 1% of the
human genome. HERVs have retained the potential of other retroelements
to retrotranspose and thus to change genomic structure and function.
The genomes of almost all HERV families are highly defective. Recent
progress has allowed the identification of the biologically most
active family, HTDV/HERV-K, which codes for viral proteins and
particles and is highly expressed in germ-cell tumors. The
demonstrable and potential roles of HTDV/HERV-K as well as of other
human elements in disease and in maintaining genome plasticity are
illustrated.

Full article available at:
http://www.pubmedcentral.nih.gov/art...bmedid=8643549


Well, this is ancient and silly. Where in this paper does it 'prove"
that none of the HIV proteins tested belong to HIV? How absurd! HIV's
genome has been sequenced, expressed and analyzed. If the abundant
data from labs all over the planet that can undertake this type of
research are ALL lying, then all of virus research is wrong. Indeed,
you are entitled to believe any nonsense you like but that really is
beyond the pale for being idiotic.

This cite refers to a website:
http://www.virusmyth.net/aids/data/cjtestfp.htm
an old article by Christine Johnson. Didn't she die of AIDS?

Pregnancy may cause a false positive on ELISA which is why a Western
Blot is utilized. A viral load test can also be used to confirm
infection, as well as evaluation of CD4 count and clinical condition.
See, e.g.,
http://www.health.arizona.edu/Health...iv_booklet.pdf
http://www.sogc.org/pub_ed/HIVtest/index_e.shtml

and in general regarding testing again, see:
http://hivinsite.ucsf.edu/InSite.jsp?doc=2098.3075


Nonsense. "Nullifying"? This is just a vacuous opinion not supported
by the very data you cite.

Cite 75 is
http://www.pubmedcentral.nih.gov/art...bmedid=8643549
is the same as 74 above regarding HERVs. Cite 109 is from the
discredited "Perth group". I am discounting them because they claim
HIV doesn't exist and this is just too stupid to waste more time on.
(Don't believe me, if you are a denialist, ask Peter Duesberg.)

On what basis is it claimed that neither England nor Wales use Western
blot as a follow up?

This is a letter: de Mendoza C, Holguin A, Soriano V. False positives
for HIV using commercial viral load quantification assays.

False positives can happen in any test. Irrelevant comment.

Every test can give false negatives.

Every test can give false positives.
Cite 113 is http://www.virusmyth.net/aids/data/miloads.htm
A long article I will have to read later...

(36) Annals of Internal Medicine 1996, 124:803-815
(37) J. of AIDS and Human Retrovirology 1997, 15(2):174-5
(38) J. AIDS 1992, 5(9):872-877
An old cite.

In general, sensitivity and specificity is pretty damn high for PCR
compared to MANY tests. Syphilis tests can be pretty dismal, but that
doesn't mean that syphilis doesn't exist or cause disease.

Again, such disingenuous observations are not inconsistencies.

OK--I will pick up actually on these last two points tomorrow.

So far, this list is batting zero.

George M. Carter

On Wed, 07 Apr 2004 11:53:29 GMT, GMCarter <fiar@verizon.net> wrote:

Indeed...an addition. The letter is available on line. See below. This
does NOT support your comments re viral load, nor does it act as a
basis for rejecting HIV as a cause of AIDS. To the contrary, it
refutes you. Note they say:

"Although false positives have been recoganized in some studies,
retesting does not reproduce the error in most instances."

and

"Our data support the notion that viral load quantification methods
must be used for monitoring plasma HIV-1 RNA levels in patients
already known to be HIV-infected."

Basically, these data suggest that PCR not be used as a diagnostic
tool. If we ONLY had PCR or NASBA, etc., concerns could be
legitimately be raised. But we have: ELISA, Western Blot, PCR, NASBA,
heat-dissociated p24, CD4 counts and percentages, CD8 and clinical
signs and symptoms that collectively provide a far too hideous
assurance of an individual's HIV status.

Overall specificity and sensitivity of these tests is already
individually quite high. Collectively, they provide even more
assurance. Just ask David Pasquarelli.

Oh. That's right. You can't. He's dead because he bought your
bullshit.

George M. Carter

***
http://www.aidsonline.com/pt/re/aids...n1i!1871977148
AIDS: Volume 12(15) 1998 p 2076-2077
False positives for HIV using commercial viral load quantification
assays
de Mendoza, C1; Holguín, A1; Soriano, V1
1Service of Infectious Diseases, Instituto de Salud Carlos III, C/
Rafael Calvo 7, 2° A, 28010 Madrid, Spain.
Date of receipt: 19 May 1998; accepted: 26 May 1998.
A 5-month-old boy was diagnosed with severe thrombopenia. His parents
had been engaged in injecting drug use practices (sharing needles) for
long time before they married. They had declined testing for HIV
antibodies in the past, and both were currently in good health. The
paediatrician decided to examine the child's HIV serological status,
but subsequently it was suggested that he should perform a viral load
test, because the result could be available the next day and the
presence of HIV sequences rather than the detection of antibodies,
which can reflect passive transfer from the mother, is more accurate
for the diagnosis of HIV infection in newborns. The child's plasma
viral load was 3044 HIV RNA copies/ml, and he began to receive
zidovudine plus didanosine in combination once this information was
available. Unexpectedly, days later it was discovered that HIV
antibodies were not detected in sera collected from the child or from
his parents. Moreover, additional serological screening assays,
including Western blot analysis, yielded negative results for HIV
antibodies. The plasma viral load was examined in a new specimen using
the same technique (HIV Quantiplex, Chiron, Madrid, Spain) and again
it gave a positive result of 5120 HIV RNA copies/ml.

Since sporadic cases of HIV-1 infection in the absence of specific
antibodies have been reported in the literature [1-4], the presence of
several HIV genomic regions (gag, env) in the child's plasma was
examined using the PCR technique. Negative results were obtained in
all instances. Furthermore, p24 antigenaemia was also negative, and
CD4+ lymphocyte counts of the child and his parents were in the normal
range. A suspicious false-positive viral load result becomes the sole
explanation ofr this controversy.

Since viral load tests have been approved for the quantification of
viraemia in already known HIV-seropositive individuals, we were
interested to know their specificity. For this purpose, we selected 20
healthy volunteers, all of whom yielded negative results for HIV
antibodies using different screening tests. Plasma from all of them
were analysed by three different currently available HIV viral load
tests: branched DNA (bDNA) signal amplification assay (Chiron),
nucleic acid sequence-based amplification (NASBA) Nuclisens (Organon
Teknika, Barcelona, Spain), and Ultradirect reverse transcriptase
(RT)-PCR Monitor (Roche, Madrid, Spain). The detection limits of these
assays are 500, 40 and 20 HIV RNA copies/ml, respectively. Moreover,
we used two different HIV-1 Monitor kits (Roche, Madrid, Spain), one
using primers exclusively designed for recognizing HIV-1 subtype B and
another with non-B primers [4].

In summary, two samples yielded positive results by the bDNA assay,
with values of 2020 and 10 620 HIV RNA copies/ml. Another two
specimens yielded false-positive results by the NASBA Nuclisens, with
values of 150 and 480 HIV RNA copies/ml. Finally, one of the 20
samples was interpreted as positive by the Ultradirect RT-PCR Monitor
assay, with a value of 73 HIV RNA copies/ml. Moreover, using the
Monitor test with non-B primers, up to four of the 20 samples yielded
positive values, ranging from 48 to 253 HIV RNA copies/ml. Results
were reproduced in more than half of tested specimens for which plasma
volumes were enough for repeat testing. The experiments were all
performed by a single well-trained laboratory technician. Furthermore,
controls run during the study excluded contamination as a source of
false-positive results.

The performance and sensitivity of the three commercially available
viral load assays has been analysed in several comparative studies,
concluding that relatively good agreement exists when comparing the
results provided [1-3]. However, non-specific hybridization between
the probes or the primers used in the current tests has been noted.
Recently, bDNA has incorporated new molecules that lead to a
substantial reduction in unspecific hybridizations [4]. The
coamplification of internal standard nucleic acid sequences, either
DNA or RNA, has been applied successfully for RT-PCR and NASBA [5,6].
Although false positives have been recoganized in some studies,
retesting does not reproduce the error in most instances.

Short fragments of cellular RNA can be misleading, being recognized or
interfering with the amplification systems used by the different
quantification methods. Targeting other nucleic acid sequences could
lead to the amplification of background, providing false-positive
results, usually with low values, as it was seen in our cases.

Our data support the notion that viral load quantification methods
must be used for monitoring plasma HIV-1 RNA levels in patients
already known to be HIV-infected. Since their specificity is not well
known, these tests must not be used for diagnostic purposes (as has
been suggested by others) [7], substituting the well-probed
serological methods. Finally, since unspecific results may occur, the
extent to which this phenomenon can affect the values provided by
testing HIV-positive specimens, leading to an underestimation of the
real number of undetectable samples, should be examined. In light of
this, recent reports [8,9] have pointed out that some individuals show
a dramatic and sustained improvement in their CD4+ lymphocyte counts
despite remaining with detectable viraemia. It is clear that
false-positive viral load results should be excluded in these
circumstances.

References
1. Revets H, Marissens D, De Wit S, et al.: Comparative evaluation of
NASBA HIV-1 RNA QT, AMPLICOR-HIV Monitor, and QUANTIPLEX HIV RNA
assay, three methods for quantification of human immunodeficiency
virus type 1 RNA in plasma. J Clin Microbiol 1996, 34:1058-1064.
[Context Link]
2. Schuurman R, Descamps D, Weverling G, et al.: Multicenter
comparison of three commercial methods for quantification of human
immunodeficiency virus type 1 RNA in plasma. J Clin Microbiol 1996,
34:3016-3022.
[Context Link]
3. Soriano V, Gómez-Cano M, Bravo R, et al.: Comparison of three
different commercial methods for quantification of plasma HIV RNA in
clinical specimens. Antiviral Ther 1997, 2:119-120.
[Context Link]
4. Collins M, Irvine B, Tyner D, et al.: A branched DNA signal
amplification assay for quantification of nucleic acid targets below
100 molecules/ml. Nucleic Acids Res 1997, 25:2979-2984.
[Context Link]
5. Barlow K, Tosswill J, Clewley J, et al.: Analysis and genotyping of
PCR products of the Amplicor HIV-1 kit. J Virol Methods 1995,
52:65-74.
[CrossRef] [Context Link]
6. Van Germen B, Kievits T, Schukkink R, et al.: Quantification of
HIV-1 RNA in plasma using NASBA during primary HIV-1 infection. J
Virol Methods 1993, 43:177-188.
[Context Link]
7. Rich J, Dickinson B, Spaulding A, Lafazia L, Flanigan T:
Interpretation of indeterminate HIV serology results in an
incarcerated population. J Acquir Immune Defic Syndr Hum Retrovirol
1998, 17:376-379.
[Context Link]
8. Kaufmann D, Pantaleo G, Sudre P, et al.: CD4 cell count in
HIV-1-infected individuals remaining viraemic with highly active
antiretroviral therapy (HAART). Lancet 1998, 351:723-724.
[Context Link]
9. Levitz S: Improvement in CD4+ cell counts despite persistently
detectable HIV load. N Engl J Med 1998, 338:1074-1075.
[CrossRef] [Context Link]

On Sun, 04 Apr 2004 20:45:46 -0400, "PaulKing"
<aimulti@aimultimedia.com> wrote:

The deconstruction of John's list continues apace...

The point here is that ALL tests have a rate of false pos/neg. The HIV
load tests have very high specificity and sensitivity, comparatively.

Cite 113 is http://www.virusmyth.net/aids/data/miloads.htm
A long article I read and he relies heavily on the letter of de
Mendoza et al. which does not support the notion.

Again, the fact that PCR, NASBA, etc. aren't 100% doesn't invalidate
their clinical relevance, nor does it have ANY relevance to the fact
that HIV exists and, in the majority of individuals, results in the
development of AIDS. Thus, another comment that is not an
inconsistency.

(36) Annals of Internal Medicine 1996, 124:803-815
(37) J. of AIDS and Human Retrovirology 1997, 15(2):174-5
(38) J. AIDS 1992, 5(9):872-877
An old cite.



Oh, this is a completely disingenuous statement! The paper says
NOTHING of this sort. This article is one of many endeavoring to
understand how the KINETICS of CD4 replication are affected by HIV.
Indeed, while this points to an incredibly important and interesting
aspect about the HOW of HIV causing AIDS, it is not an "inconsistency"
in terms of HIV existing and causing disease, but rather a mystery of
how it does so. Again, we know VERY little about how many infectious
agents actually result in disease.

Figure 4b does NOT show no correlation between viral load and CD4
count, but rather a lack of correlation between HIV load and the
KINETICS of CD4 production. This is a completely different idea that
the author of this list did not grasp. Kinetics refers to the
"turnover" rate or the rapidity with which CD4 cells are either
replaced by production of new cells from the thymus or are replaced
via clonal expansion (memory cells dividing and making copies of
themselves). According to Hellerstein's work, "untreated HIV-1
infection is associated with a higher proportion but not a higher
absolute number of dividing CD4+ T cells." There remains considerably
controversy over this issue and there have been some heated debates.
Are more of the cells that are around in HIV+ people are dividing
memory cells rather than recent thymic emigrants (new T cells coming
from the thymus)? I wrote an overview that might help to understand
the background to this area of research:
http://www.aidsinfonyc.org/fiar/9thCROI.html

Here's the abstract:
The dynamic basis for T-cell depletion in late-stage HIV-1 disease
remains controversial. Using a new, non-radioactive, endogenous
labeling technique 1, we report direct measurements of circulating
T-cell kinetics in normal and in HIV-1-infected humans. In healthy,
HIV-1-seronegative subjects, CD4+ and CD8+ T cells had half-lives of
87 days and 77 days, respectively, with absolute production rates of
10 CD4 + T cells/l per day and 6 CD8+ T cells/l per day. In untreated
HIV-1-infected subjects (with a mean CD4 level of 342 cells/l), the
half-life of each subpopulation was less than 1/3 as long as those of
healthy, HIV-1-seronegative subjects but was not compensated by an
increased absolute production rate of CD4+ T cells. After viral
replication was suppressed by highly active antiretroviral therapy for
12 weeks, the production rates of circulating CD4+ and CD8+ T cells
were considerably elevated; the kinetic basis of increased CD4 levels
was greater production, not a longer half-life, of circulating cells.
These direct measurements indicate that CD4+ T-cell lymphopenia is due
to both a shortened survival time and a failure to increase the
production of circulating CD4 + T cells. Our results focus attention
on T-cell production systems in the pathogenesis of HIV-1 disease and
the response to antiretroviral therapy

Do read the whole paper--it is a fascinating bit of work and has been
expanded upon and addressed by other groups since it was first
published.
http://www.nature.com/cgi-taf/DynaPa...nm0199_83.html

If you are GENUINELY interested in this topic, this is a great area of
mystery and exploration that may lead to better understanding of
disease and ultimately, improved treatments and/or vaccines.

Yes. Whoop-de-doo. Most of the listed issues are temporary declines,
not a chronic, sustained loss of CD4 cells as happens in HIV
infection. The cite is:
http://www.news-gap.com/mb/sda/irwinlowcd4.htm unfortunately not
found.

Antimicrob Therapy 1996, 37(Suppl. B):171-83

Well, this paper is completely misinterpreted. Abstract below. I think
some of the authors who you guys are using to support your nonsense
should sue you for defamation.

Bird AG. Non-HIV AIDS: nature and strategies for its management. J
Antimicrob Chemother. 1996 May;37 Suppl B:171-83.

Department of Immunology, Churchil Hospital, Oxford, UK.

Despite initial claims to the contrary, a cluster of reports of severe
opportunistic infections occurring in patients without evidence of HIV
infection do not appear to represent a new disease entity or present
evidence of epidemiologically associated cases suggesting an
infectious agent. Reported cases are reviewed and appear to represent
a heterogeneous group, many of which may represent sporadic cases of
late onset acquired immunodeficiency. In addition, a small group of
asymptomatic subjects have been identified with constitutively low CD4
T cell populations which appear to have little or no clinical
significance since these patients have no evidence of clinical
immunodeficiency. Newly identified cases should be fully investigated
immunologically and virologically after recovery from their presenting
infection and continuous or prophylactic therapy instituted only in
cases of substantiated long-term severe immunodeficiency.

Nonsense. Of course, ANYTHING is probably a "risk factor" and would be
rejected. But then this is predicated on a notion that HIV negatives
are all 100% free of the same (unlisted) risk factors.

But there are many studies that have looked at CD4 counts in HIV+ and
HIV- individuals. The latter have a range of counts generally around
600-1200 for CD4+ numbers. The HIV+ groups have steadily declining
numbers (down to zero). An interesting review paper:

Maecker HT, Maino VC. T cell immunity to HIV: defining parameters of
protection. Curr HIV Res. 2003 Apr;1(2):249-59.

BD Biosciences, Immunocytometry Systems, 2350 Qume Drive, San Jose, CA
95131, USA. holden_maecker@bd.com

In recent years, CD4 and CD8 T cell responses to HIV and SIV infection
have been increasingly measured with the use of single-cell assays
such as ELISPOT, MHC-peptide oligomers, and cytokine flow cytometry.
The results of these assays have been compared to those obtained with
traditional bulk assays such as lymphoproliferation (by 3H-thymidine
incorporation) and cytotoxicity (by 51Cr release). Such comparisons
have led to some general understanding of the T cell responses that
characterize progressive disease, long-term non-progressors, and
individuals with viral suppression achieved by anti-retroviral
therapy. In addition, prophylactic and therapeutic vaccine trials have
also begun to use these assays of T cell immunity to gauge the
immunogenicity of the vaccines. Whether such analyses will allow us to
pick the best vaccine constructs, and whether they will provide us
with an improved understanding of what constitutes protective cellular
immunity to HIV, are major questions for the field. These questions
will be examined in this review from the standpoint of current data
and comparisons to other viral diseases. It is hypothesized that
sophisticated multiparametric assays will be required to sort out the
factors relevant for protective immunity in this complex disease.
These parameters may include functional avidity, epitope breadth and
specificity, proliferative capacity, cytokine repertoire, degree of
anergy, and differentiation phenotype, as well as magnitude, of
HIV-specific CD4 and CD8 T cells.


Yep. This is a surprise? But the epidemic was ALSO among intravenous
drug users, very rapidly. This because there is a porosity between
"groups" which have always had fragmentary borders. Bisexual behavior
acts as a bridge between "groups." Intravenous drug use is found in
people of all sexual orientations. This is another meaningless comment
that does not act as an inconsistency nor does it refute the evidence
that HIV exists and, in the majority of infected individuals, causes
AIDS.


I have not reviewed these articles. Taking this statement at face
value (which I think is dicey considering the distortions seen to
date), it does not serve as an inconsistency in any fashion. A
sexually transmitted disease will have varying patterns of emergence.

Without a clearer explanation of how this is an inconsistency, the
point is rejected.

HAHAHAHA. This is funny.
Durex Global Sex Survey 2001, see also
http://www.mcsweeneys.net/links/press01/sex.html

A survey by a condom company?? LOL. This is funny. It is unclear, in
any event, how they acquired their data, what their sample was, who
was interviewed, etc.

Anyway, this again is not an inconsistency. IF it is accurate, it
merely means that the fertile ground for a more rapid dissemination of
HIV may arise in the US. As it has been in communities of color.

Oh for god's sakes, this sounds like that jackass, Cardinal Trujillo.
Do you understand the concept "surface tension"?

Ever filled a condom with water? (Placed in a bra, they make great,
soft breasts for dressing up in drag!)

Guess how big a water molecule is? Compared to an HIV?

I should just stop here with this level of stupidity.

While these findings may seem counterintuitive, it does not suggest in
the slightest that HIV does not exist or does not cause AIDS.

The study found that STD control efforts are successful and helpful.
However, the incidence (new infections) did not differ between groups.
The incidence was 1.5% in both groups. It may be that this level is
too low to show an effect. Syphilis lesions, though, SHOULD be treated
and may well contribute to HIV infection of a partner. That's a
no-brainer. But here, the intervention was evaluation and treatment of
STDs, not necessarily condom use or other means to prevent HIV or
other STDs. It doesn't mean condoms don't dramatically reduce the risk
of HIV infection: they do.

Abstract below:

Lancet. 1999 Feb 13;353(9152):525-35. Related Articles, Links


Comment in:
Lancet. 1999 Feb 13;353(9152):513-5.
Lancet. 1999 May 1;353(9163):1522-3; author reply 1523-4.
Lancet. 1999 May 1;353(9163):1522; author reply 1523-4.
Lancet. 1999 May 1;353(9163):1523-4.
Lancet. 2000 Nov 4;356(9241):1602-3.

Control of sexually transmitted diseases for AIDS prevention in
Uganda: a randomised community trial. Rakai Project Study Group.

Wawer MJ, Sewankambo NK, Serwadda D, Quinn TC, Paxton LA, Kiwanuka N,
Wabwire-Mangen F, Li C, Lutalo T, Nalugoda F, Gaydos CA, Moulton LH,
Meehan MO, Ahmed S, Gray RH.

Centre for Population and Family Health, Columbia University School of
Public Health, New York 10032, USA.

BACKGROUND: The study tested the hypothesis that community-level
control of sexually transmitted disease (STD) would result in lower
incidence of HIV-1 infection in comparison with control communities.
METHODS: This randomised, controlled, single-masked, community-based
trial of intensive STD control, via home-based mass antibiotic
treatment, took place in Rakai District, Uganda. Ten community
clusters were randomly assigned to intervention or control groups. All
consenting residents aged 15-59 years were enrolled; visited in the
home every 10 months; interviewed; asked to provide biological samples
for assessment of HIV-1 infection and STDs; and were provided with
mass treatment (azithromycin, ciprofloxacin, metronidazole in the
intervention group, vitamins/anthelmintic drug in the control).
Intention-to-treat analyses used multivariate, paired,
cluster-adjusted rate ratios. FINDINGS: The baseline prevalence of
HIV-1 infection was 15.9%. 6602 HIV-1-negative individuals were
enrolled in the intervention group and 6124 in the control group.
75.0% of intervention-group and 72.6% of control-group participants
provided at least one follow-up sample for HIV-1 testing. At
enrolment, the two treatment groups were similar in STD prevalence
rates. At 20-month follow-up, the prevalences of syphilis (352/6238
[5.6%]) vs 359/5284 [6.8%]; rate ratio 0.80 [95% CI 0.71-0.89]) and
trichomoniasis (182/1968 [9.3%] vs 261/1815 [14.4%]; rate ratio 0.59
[0.38-0.91]) were significantly lower in the intervention group than
in the control group. The incidence of HIV-1 infection was 1.5 per 100
person-years in both groups (rate ratio 0.97 [0.81-1.16]). In pregnant
women, the follow-up prevalences of trichomoniasis, bacterial
vaginosis, gonorrhoea, and chlamydia infection were significantly
lower in the intervention group than in the control group. No effect
of the intervention on incidence of HIV-1 infection was observed in
pregnant women or in stratified analyses. INTERPRETATION: We observed
no effect of the STD intervention on the incidence of HIV-1 infection.
In the Rakai population, a substantial proportion of HIV-1 acquisition
appears to occur independently of treatable STD cofactors.

This is an uncited comment. The proportion of the total population
being tested is not the issue, at any rate. It is the number of
at-risk individuals. And testing is fairly wide-spread.

This is repeating points made previously. The testing issue needs to
be addressed. Many places in Africa DO provide Western blot follow up.

It doesn't mean HIV doesn't exist or doesn't cause AIDS.

Relevance? A letter from: Stuart W Dwyer, part time district surgeon
(forensic medical officer). Hardly a rigorous epidemiological survey
of the extent of HIV in South African prisons and jails.

That's enough today.

Two-thirds done and still, there is nothing in this list that refutes
the fact that HIV exists or causes AIDS.

Indeed, some interesting points are raised. Controversies exist with
regard to how AIDS develops. One point that I haven't seen yet is that
many CD4 cells that die are not infected. There are many mechanisms
being addressed to understand how this arises--and I believe oxidative
stress plays a key role in that aspect of HIV disease. Which is why I
think antioxidant therapy is a part of a complete regimen.

There IS more to HIV/AIDS than antiviral therapy! But to pretend it
doesen't exist risks people having sex without condoms. And acquiring
HIV. It risks people avoiding treatment by staying in denial. And
dying like Pasquarelli did. Taking ARV is no guarantee, of course. My
friend Keith died the other night. My friends Evan and Carlton died
last November. They fought hard.

There IS much more to learn. But playing this denialist game is
lethally stupid.

More tomorrow.

George M. Carter

Top 100 AIDS Science Inconsistencies
By John Kirkham
http://www.altheal.org/science/top100.html

All of the observations below can be substantiated by independent
research. How long can the HIV=AIDS=Death dogma be maintained in the
face of so many scientific cracks?

1. AIDS occurs in the absense of HIV (65, 87), a new medical
definition (Idiopathic CD4+ T-cell lymphocytopenia) was therefore
created.
2. HIV does not satisfy Koch's postulates, the criteria that must
be met in order to prove that a microbe causes a disease (90)
3. Anti-HIV drugs, including protease inhibitors, destroy T-cells
(4-10)
4. Septrin (also called Septra, Bactrim, Co-trimoxazole) and
anti-HIV drugs destroy mitochondria (11,12)
5. The PCP (Pneumocystis Carinii pneumonia) fungus becomes
resistant to Septrin (12)
6. Recreational drugs (heroin, poppers, crystal met, ecstasy,
cocaine) reduce CD4 cell numbers (13-18, 58, 66-68)
7. HIV positive patients recover after they stop taking drugs (58)
8. Recreational drugs cause AIDS-defining diseases (see table 7 of
58)
9. Anti-HIV drugs cause AIDS-defining diseases (58)
10. Anti-HIV drugs inhibit human enzymes (11)
11. HIV positive Africans in dire poverty in Uganda and no access
to anti-HIV drugs lived as long as HIV positives in the West who took
anti-HIV drugs (33)
12. There are no comparative studies of survival in HIV negatives
and combo-free HIV positive heterosexuals with no other risk factors.
13. Only 38% of healthy long-term positives had ever used AZT or
other nuleoside analogs compared with 94% of progressors (80)
14. Decreases in AIDS cases preceded the introduction of new drug
treatments (Dec 1995) by three full years (see fig. 6 of 106)
15. Anti-HIV drugs have anti-microbial effects (49, 50, 10)
16. The introduction of AZT did not cause a decline in the AIDS
death rate (105)
17. In the only long term trial of AZT (The Concorde study) 172
participants died, 169 while taking AZT, 3 while on placebo (51)
18. Nucleoside analog drugs suppress/destroy the bone marrow where
all immune system cells are born (26, 32, 111)
19. HIV+ children born to AZT treated mothers had a higher
probability of developing severe disease or severe immunsuppression
(53)
20. "Drug holidays" recover immune responses
21. AZT caused the same transient increase in CD4 count in HIV
negatives as in HIV positives (55)
22. There are no controlled studies showing that AIDS occurs in the
absense of all other possible non-HIV causal factors.
23. Long-living, healthy, drug-free HIV positives are mostly
ignored by AIDS researchers
24. Apart from the early (fraudulent) AZT studies and the Concorde
study no efficacy studies compare drugs with placebo
25. There are well documented, non-HIV causes for every AIDS
disease
26. The incidence of AIDS-defining diseases among Western non-drug
users has not been shown to exceed national backgrounds (58)
27. Early AIDS coincided with the cumulative effects of
unprecedented, intense use of volatile nitrite (poppers) as a
aphrodisiac marketed almost exclusively to homosexuals (102)
28. AIDS can be treated effectively without anti-HIV drugs (39-42,
112)
29. On average viral load overestimates infectious HIV by a factor
of 60,000 (21)
30. Even a PCR method that can detect 1 infected cell in 100000
found very little HIV DNA in HIV positives (23)
31. HIV could not be cultured from people with a detectable viral
load (19, 21)
32. HIV has never been properly isolated (20)
33. After many billions of dollars of research effort over 20
years, HIV scientists still cannot explain how HIV causes AIDS.
34. After many billions of dollars of research effort over 20 years
there is no vaccine and no cure, there are only toxic drugs
35. There was no increase in HIV seroprevalence outside risk groups
in the UK despite record STD rates and teenage pregnancy rates (25)
36. HIV DNA was found to be constant from the time of
seroconversion but CD4 count continually went down (29)
37. CD4 count goes down and viral load goes up while on the
anti-HIV drugs.
38. AZT is hardly triphosphorylated by the body so it cannot
possibly have an anti-HIV effect (30)
39. AZT has no effect on HIV DNA but makes viral load (HIV RNA) go
down (31)
40. Research throughout the 1970s showed that retroviruses do not
kill cells.
41. The probability of heterosexual transmission of HIV was found
to be very low (1 in a 1000 for male to female and 8 times less likely
for female to male) (34)
42. HIV antibody tests can give repeated false positives and
seroreversions can occur (95-100, 114-116)
43. HIV tests are sensitive to non-specific antibody binding
44. HIV tests involve an arbitrary dilution factor, everyone tests
positive (because of non-specific antibody binding) if their serum is
undiluted (104)
45. All the proteins used in the HIV test are associated with
retroviral genes that are found naturally (endogenous) in all humans
(72)
46. Endogenous retroviruses can generate immune responses in humans
(73, 74)
47. None of the HIV proteins tested for have been proven to belong
to HIV (75)
48. There are over 60 different conditions, including pregnancy,
that have been known to generate false positives on the HIV test (91)
49. The Elisa, Western Blot and PCR tests for HIV all carry
disclaimers nullifying their detection of HIV
50. The criteria for HIV-positivity used in the antibody tests
varies between countries and between organisations within a country and
can produce indeterminate (neither positive or negative) results (75,
109) The Western Blot HIV test, widely regarded as the most accurate,
is not used in England and Wales because it is regarded as inaccurate.
51. The viral load PCR primers were found to be non-specific for
"HIV" genetic sequences (35)
52. The viral load test gives false negatives (36)
53. The viral load test gives false positives (36, 113)
54. The viral load test has low reproducibility (36-38)
55. Direct measurements showed no correlation between viral load
and CD4 count (43)
56. Many conditions cause reduced CD4 counts (86)
57. CD4 counts between 200 and 300 have been observed in healthy
HIV negatives (87)
58. There are no studies comparing CD4 cell variations in
combo-free HIV positives (with no risk factors) and HIV negatives.
59. According to the AIDS establishment, a heterosexual AIDS
"epidemic" of African origin started off in the West as a homosexual
"epidemic"
60. In 1985 HIV incidence in Southern Africa was confined to
homosexuals who had been to the US and those who had had sex with them
(88, 89).
61. The USA was found to be the world's most sexually promiscuous
nation (27)
62. Condoms (made from polyisoprene) have holes in much larger than
HIV (28, 110)
63. Reducing STD incidence in Africa did not reduce the rate of HIV
seroconversion* (101)
64. Only a minute proportion of Africans have actually been tested
for HIV, seroprevalence estimates are derived from extrapolations based
on unrepresentative samples from maternity clinics.
65. In Africa a single positive ELISA test or even a single "rapid"
(saliva/urine) test is considered proof of HIV infection, "proof" in
the developed world requires a series of tests
66. HIV seroprevalence was found to be much lower in South African
prisons than in the general population (1)
67. The vast majority of African "AIDS patients" tested HIV
negative (44, 45)
68. In "AIDS ravaged" Zambia since 1980 the population has
increased and even the rate of increase in population has increased!
(46)
69. In "AIDS ravaged" South Africa many coffin makers are either
doing a slack trade or have gone out of business (47)
70. The total number of AIDS cases in Africa consists almost
entirely of estimated cases rather than known, registered cases (54)
71. PCP is the typical AIDS defining disease in Western adults but
it is almost entirely confined to young children in Africa (2,3)
72. There is no Western heterosexual AIDS epidemic
73. IVDUs who consistently used a clean needle exchange program
were 10.2 to 22.9 times MORE likely to test HIV positive than non-users
(48)
74. Non-human primates "progress" to AIDS (SAIDS) much quicker than
humans do (107)
75. SIV does not cause SAIDS in wild primate populations (108)
76. SIV seroprevalence is too low in wild primate populations to
account for SIV resistance in these populations (22)
77. SIV seroprevalence in captive SIV naïve primate populations
was found to be very low (22)
78. Until the early 1930s many thousands of European men received
transplants from chimpanzees and did not get AIDS (62)
79. Uganda study showed HIV-positivity did not indicate a new cause
of disease, only decreased mortality in HIV negatives (52)
80. One thousand medical staff a year accidentally contract
hepatitis from needles yet by 1998 there were no documented cases of
surgeons or emergency medical technicians/paramedics getting AIDS, or
even HIV, from occupational exposure (58, Table 16 of 106)
81. All AIDS patients have lowered levels of glutathione, the major
water soluble intracellular antioxidant (59, 60)
82. The antioxidant N-acetyl cysteine inhibits "HIV replication"
(61)
83. Reactive oxygen species are implicated in the induction of HIV
expression and cell death (40)
84. Treatment with oxidising, mitogenic*** agents is necessary for
HIV "isolation" from cell culture (56, 57)
85. Significant HIV replication was found to follow rather than
precede AIDS defining disease (94)
86. Low T-cell counts were shown to occur before HIV seroconversion
and to predict seroconversion (92, 93)
87. HIV-like genetic sequences have been found in the HIV negative
human genome (63)
88. Epitopes** of HIV regulatory proteins tat, rev and nef are
expressed in normal human tissue (71, 116)
89. Toxic intracellular stresses can create novel genetic sequences
(64)
90. HIV showed over 40% variation in an essential gene (protease)
sequence within a single subtype (103)
91. Foreign protein transfusions were found to be immune
suppressive (79, 81, 84, 85)
92. Hemophiliacs can have hypergammaglobulinaemia which can cause
false HIV positive test results (69)
93. Up to 99.9% of HIV genomes in plasma may be defective (70)
94. Mortality in hemophiliacs began to increase in exactly the same
year they began taking AZT (81, 82)
95. The AIDS risk of hemophiliacs on AZT was 4.5 times higher, and
mortality 2.4 times higher, than untreated controls (83)
96. Infectious HIV (a delicate virus) does not survive the Factor
VIII preparation process (76-78)
97. HIV theorists have made incorrect predictions throughout the
HIV era.
98. Corticosteroids and endogenous cortisol suppress cellular
immune responses and cortisol destroys immature T-cells (24)
99. Effective cellular immunity relies upon nitric oxide gas
defence, see for example Eur. J. Immunol. 2002, 32(5):1455-63
100. AIDS spreads non-exponentially, unlike infectious disease (58)

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Footnotes

*Conversion from HIV negative to HIV positive
**Epitopes are part of a molecule against which antibodies are made
***Stimulates cell division

John Kirkham : kirkhamjohn@hotmail.com
Website : http://www.geocities.com/pharmharm

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100 of at least 10,000.

Nothing about 'AIDS' makes any sense.

"George DeCarlo" <alexdn@ix.netcom.com> wrote in message
news:1110052720.196510.25430@z14g2000cwz.googlegro ups.com...
Top 100 AIDS Science Inconsistencies
By John Kirkham

Here are some answers to all of the so called "Inconsistencies";

http://ww2.aegis.org/default.asp?req...DS_Debate.html

http://www.niaid.nih.gov/Publications/hivaids/20.htm

http://www.niaid.nih.gov/Publications/hivaids/13.htm

http://www.hivpositive.com/f-HIVyou/...ausesAIDS.html

http://www.niaid.nih.gov/factsheets/howhiv.htm

http://www2.niaid.nih.gov/Newsroom/F...0/MACSWIHS.htm

http://www.quackwatch.org/04Consumer.../hiv-aids.html

http://www.avert.org/evidence.htm

http://www2.niaid.nih.gov/Newsroom/F...00/default.htm

Gary Stein