Douglas Richman of UC San Diego was the investigator of ACTG019
and has part of the Volberding-Saag-Fischl et al Death Squad
that appointed itself the responsibility to define the AIDS
"Standard of Care" — these selfless beings of light have
been poodles for the drug companies from day #1. Richman is the
senior author of the first article.

It is interesting that Richman submitted this research on July 6,
1996 for publication in the Journal of Virology. This was right
around the time of the Victory in Vancouver Circus — yet the many
insights in this research were quite contrary to the Drugfest
propaganda. At the very least, this information would have ruined
everyone’s good time (if it was put in the context of the combo
drugs) since it establishes the basis upon which HIV can and
will elude these toxic chemotherapies in any combination that
still leaves the patient breathing (albeit with non-functioning
kidneys, liver, adrenals and circulatory disease). Everyone
seems to forget that medicine has never eliminated a virus from
a human being by using a drug — not the flu, cold, or anything
else. The best hope (probably the only hope) lies in the
area of immune-based research — which seems to be a rather low
priority given the promotional hysteria present in the combo
cocktail community today. I suppose that’s the price to be
paid for a focus on quick-fix drug cures — a focus that has
led the treatment community down another blind alley while
10 years drifted by.

The ever-shifting drug-promoting paradigm shows why the concept
of "resistance" is absurd (it used to be blamed on "mutants"
until they got busted on that one — the mutants were just
normal HIV variants… sorry). The statements below should be
carefully examined — the message is devastating to the
10-year old Model of Treatment that was obsoleted 10 years
ago, simply because it was built on a Model of Pathogenesis
that was also obsolete 10 years ago — the drug apologists
keep trying to patch up their model of pathogenesis to hold
up the ever-collapsing model of treatment. Watching them
hammer those square pegs in the round holes gets more amusing
each time they get ever-bigger square pegs (that is, contradictory
discoveries). This, of course, is known as the "reverse engineering"
of the old treatment paradigm to match the new disease realities.
The current drug treatments are not based on objective science —
but rather pure nonsense, greed, inflated egos and madness.

fred

——-

Billi Goldberg offers the following:

Very interesting pair of articles in the March 1997 issue of the Journal
of Virology. Contents and abstracts available at website
www.asmusa.org/jnlsrc/journal.htm.

Richman’s group found that the virus mutates differently in different
compartments. They state that "Selective pressures within the
microenvironments of different anatomic compartments result in the
emergence of dominant quasispecies which can be distinguished by their
envelope sequences," AND "Moreover, brain-derived sequences appeared to
be phylogenetically distinct from spleen- and lymph node-derived
sequences even after exclusion of resistance codons from analysis," AND
"These observations support the concept of anatomically distinct,
independently evolving quasispecies (virodemes)."

Is there the possibility that different antiviral regimes will be
required for the different anatomic compartments?

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

In Vivo Compartmentalization of Human Immunodeficiency Virus: Evidence
from the Examination of pol Sequences from Autopsy Tissues.

Joseph K. Wong, Caroline C. Ignacio, Francesca Torriani,
Diane Havlir, Nicholas J. S. Fitch, and Douglas D. Richman.

Journal of Virology, Mar. 1997, Vol. 71, No. 3, p. 2059-2071

Abstract: High rates of mutation and replication of human
immunodeficiency virus (HIV) allow for the continuous generation of
diverse genetic variants in vivo. Selective pressures within the
microenvironments of different anatomic compartments result in the
emergence of dominant quasispecies which can be distinguished by their
envelope sequences. It is not known whether comparable tissue-specific
selective pressures lead to the independent evolution of pol sequences
within different tissue compartments, nor is it known how differing
rates of virus turnover in tissues might affect the pace of such
evolution. These issues are of importance for the formulation of a model
for the emergence of drug resistance in vivo and for a general
understanding of virus trafficking and virus turnover. Regions of the
HIV type 1 reverse transcriptase (RT) which carry the majority of the
known resistance codons to RT inhibitors (700 nucleotides from each
clone) were cloned and sequenced directly from autopsied brain, spleen,
and lymph node specimens from four subjects who had received zidovudine
therapy. Clones from proviral DNA (143) and from viral cDNA (14) were
analyzed. In three of four subjects, a discordance in distribution of
resistance codons was noted. Moreover, brain-derived sequences appeared
to be phylogenetically distinct from spleen- and lymph node-derived
sequences even after exclusion of resistance codons from analysis. In
each case, evidence for differential immune selective pressure, based on
comparison of inferred amino acid sequences corresponding to known major
histocompatibility complex class I cytotoxic T-lymphocyte epitopes, was
found. These observations support the concept of anatomically distinct,
independently evolving quasispecies (virodemes).

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