"DavidT" <david199@volcanomail.com> wrote in message

Once it can be demonstrated that there is a false premises
every-thing that follows has to be incorrect.

Creditability is thrown away for an agenda.

Regarding the lack of  value in reducing surrogate HIV RNA viral load
markers with toxic drugs:

This Lancet article shows that HAART  treatment of HIV can produce
improvement in surrogate markers such as reduction in viral load (HIV
RNA  PCR), however, "but such improvement has not translated into a
decrease in mortality" (author's quote) (1)

Not only that, but this JAMA article shows that HIV viral load markers
cannot even predict which individual HIV positives will have CD4 cell
count decline (which is the current definition of AIDS). (2)

Of course, this is old news, since others such as Hogg, have shown
that HIV RNA Viral Load Surrogate markers, were not significant. "
Only CD4 cell count remained statistically significant in the
multivariate analysis of progression to death". (author's quote) (3)

The reason for this is that unlike the human influenza A virus (4),
death from AIDS is NOT associated with high plasma viremia.  In fact
it is extremely difficult to demonstrate HIV virus in the blood of
AIDS patients. That's why reliance is placed on the RNA PCR test which
amplifies tiny amounts RNA.  And  why after 20 years of research and
100 B NIH dollars, there are still serious questions about the entire
HIV causes AIDS hypothesis.  However, the money pot is so large and
tempting; the HIV causes AIDS blunder must continue.  How many
messages on the internet are posted by paid shills for the drug
industry or by member of the research community who are funded by the
NIH ?  That funding dries up once the blunder is admitted.

David Pratt sums it up quite well:

"A person's 'viral load' is determined by means of the polymerase
chain reaction (PCR) test. But this test does not detect actual virus.
It amplifies millions of times small genetic segments assumed to be
associated with 'HIV' so that they become detectable, and these
fragments of genetic material are then assumed to correspond to counts
of actual virus. Using this method, an average of over 100,000 HIVs
per millilitre of blood are found in AIDS patients. However, when
standard virus-counting methods, are applied, a viral load of 100,000
is found to correspond to less than 10 infectious units of HIV - far
too little to induce illness.

Viral loads have been measured in people who are HIV-negative and in
AIDS patients who test HIV-antibody positive but have no HIV. Low
viral loads do not correlate with high T-cell counts or good health,
while high viral loads do not correspond with low T-cell counts or
sickness. Kary Mullis, who won the Nobel Prize in 1993 for inventing
PCR, says that the conclusions being drawn from PCR's use in these
tests are worthless. Some critics have bluntly characterized this new
hypothesis as 'a viral load of crap'."

references:

(1) http://tinyurl.com/2tcpgx

"INTERPRETATION: Virological response after starting HAART improved
over calendar years, but such improvement has not translated into a
decrease in mortality."

HIV treatment response and prognosis in Europe and North America in
the first decade of highly active antiretroviral therapy: a
collaborative analysis. Lancet

(2) http://jama.ama-assn.org/cgi/content/abstract/296/12/1498

Predictive Value of Plasma HIV RNA Level on Rate of CD4 T-Cell Decline
in Untreated HIV Infection Benigno Rodríguez,

(3) http://jama.ama-assn.org/cgi/content/abstract/286/20/2568

Rates of Disease Progression by Baseline CD4 Cell Count and Viral Load
After Initiating Triple-Drug Therapy

Robert S. Hogg, PhD; Benita Yip, BSc(Pharm); Keith J. Chan, MSc; Evan
Wood, BSc; Kevin J. P. Craib, MMath; Michael V. O'Shaughnessy,
OBC,PhD; Julio S. G. Montaner, MD,FRCPC,FCCP

JAMA. 2001;286:2568-2577.

Context  Current recommendations for initiation of antiretroviral
therapy in patients infected with human immunodeficiency virus type 1
(HIV) are based on CD4 T-lymphocyte cell counts and plasma HIV RNA
levels. The relative prognostic value of each marker following
initiation of therapy has not been fully characterized.

Objective  To describe rates of disease progression to death and AIDS
or death among patients starting triple-drug antiretroviral therapy,
stratified by baseline CD4 cell count and HIV RNA levels.

Design, Setting, and Participants  Population-based analysis of 1219
antiretroviral therapy-naive HIV-positive men and women aged 18 years
or older in British Columbia who initiated triple-drug therapy between
August 1, 1996, and September 30, 1999.

Main Outcome Measure  Cumulative mortality rates from the initiation
of triple-drug antiretroviral therapy to September 30, 2000,
determined using various CD4 cell and plasma HIV RNA thresholds.

Results  As of September 30, 2000, 82 patients had died of AIDS-
related causes, for a crude AIDS-related mortality rate of 6.7%. The
product limit estimate (SE) of the cumulative mortality rate at 12
months was 2.9% (0.5%). In univariate analyses, a prior diagnosis of
acquired immunodeficiency syndrome (AIDS), CD4 cell count, use of
protease inhibitors, and HIV RNA level were associated with mortality.
There was no difference in mortality by age or sex. Only CD4 cell
count remained statistically significant in the multivariate analysis.
After controlling for AIDS, protease inhibitor use, and plasma HIV RNA
level at baseline, patients with CD4 cell counts of less than 50/µL
were 6.67 (95% confidence interval [CI], 3.61-12.34) times and those
with counts of 50/µL to 199/µL were 3.41 (95% CI, 1.93-6.03) times
more likely to die than those with counts of at least 200/µL.

Conclusion  Our data demonstrate uniformly low rates of disease
progression to death and AIDS or death among patients starting
antiretroviral therapy with CD4 cell counts of at least 200/µL. In our
study, disease progression to death and AIDS or death was clustered
among patients starting therapy with CD4 cell counts less than 200/
µL.

(4) http://www.nature.com/nm/journal/v12/n10/abs/nm1477.html

Nature Medicine - 12, 1203 - 1207 (2006)

Fatal outcome of human influenza A (H5N1) is associated with high
viral load and hypercytokinemia

Menno D de Jong1, Cameron P Simmons

Avian influenza A (H5N1) viruses cause severe disease in humans1, 2,
but the basis for their virulence remains unclear. In vitro and animal
studies indicate that high and disseminated viral replication is
important for disease pathogenesis3, 4, 5. Laboratory experiments
suggest that virus-induced cytokine dysregulation may contribute to
disease severity6, 7, 8, 9. To assess the relevance of these findings
for human disease, we performed virological and immunological studies
in 18 individuals with H5N1 and 8 individuals infected with human
influenza virus subtypes. Influenza H5N1 infection in humans is
characterized by high pharyngeal virus loads and frequent detection of
viral RNA in rectum and blood. Viral RNA in blood was present only in
fatal H5N1 cases and was associated with higher pharyngeal viral
loads. We observed low peripheral blood T-lymphocyte counts and high
chemokine and cytokine levels in H5N1-infected individuals,
particularly in those who died, and these correlated with pharyngeal
viral loads. Genetic characterization of H5N1 viruses revealed
mutations in the viral polymerase complex associated with mammalian
adaptation and virulence. Our observations indicate that high viral
load, and the resulting intense inflammatory responses, are central to
influenza H5N1 pathogenesis. The focus of clinical management should
be on preventing this intense cytokine response, by early diagnosis
and effective antiviral treatment.

(5) http://ourworld.compuserve.com/homepages/dp5/aids.htm