Notorious Internet swindler Clyde Bell from the State of Tennessee, who stole
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Congratulations to all users of the Internet with the Victory of the  State
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http://www.icis.net/fourone -> SHOP TALK -> "Fraud through Internet"
or
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We suggest to let as many Internet users know about this as possible. Everyone
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Four One Company Ltd

I produce a cable tv program on alternative health, called
"Accent on Wellness" that airs Saturday mornings in Manhattan.

In nearly four years we’ve built a large, loyal following.
Received an interesting call from a viewer who was in Lenox Hill
Hospital, one of NY’s leading hospitals, last Saturday.  He was tuned in
at 7:30 in the morning and saw the preview screen, "Coming up at 7:30
‘Accent on Wellness’", but when the show should have come on, the channel
automatically changed to something else.

No folks, this isn’t Russia, or Nazi Germany, it’s Lenox Hill Hospital in
the City of New York, is Clinton’s good old US of A.  Kiss your rights
goodbye folks.  The gestapo is back.

Edward Lieb
forl…@panix.com

         __ o
       _`\ <,_
______(*)/  (*)____________________________

What if everything that you thought you knew about AIDS was wrong?

    ***Visit HEAL on the Worldwide Web:

           www.aidsnyc.org/heal/index.htm

Want to learn how people cure themselves of cancer, AIDS, etc?

Ask for the free report "Bounce Back to Health" from HelthBo…@aol.com

Chemokine receptors get more and more interesting and confusing.

He et al. show that CCR3 and CCR5 can be used as receptors to infect
microglia.

Ditmar et al. summarize the confusion by stating "We show here that it
is oversimplistic to assume that chemokine co-receptor use accurately
reflects the cellular tropism of the virus."

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

J He, Y Chen, M Farzan, H Choe, A Ohagen, S Gartner, J Busciglio, X
Yang, W Hofmann, W Newman, C R Mackay, J Sodroski & D Gabuzda.
CCR3 and CCR5 are co-receptors for HIV-1 infection of microglia (Letter
to Nature of 2/13/97). Nature 385, 645 (1997).

Abstract: Several members of the chemokine receptor family are used
together with CD4 for HIV-1 entry into target cells. T cell line-tropic
(T-tropic) HIV-1 viruses use the chemokine receptor CXCR4 as a
co-receptor, whereas macrophage-tropic (M-tropic) primary viruses use
CCR5. Individuals with defective CCR5 alleles exhibit resistance to
HIV-1 infection, suggesting that CCR5 has an important role in vivo in
HIV-1 replication. A subset of primary viruses can use CCR3 as well as
CCR5 as a co-receptor, but the in vivo contribution of CCR3 to HIV-1
infection and pathogenesis is unknown. HIV-1 infects the central nervous
system (CNS) and causes the dementia associated with AIDS. Here the
authors report that the major target cells for HIV-1 infection in the
CNS, the microglia, express both CCR3 and CCR5. The CCR3 ligand,
eotaxin, and an anti-CCR3 antibody inhibited HIV-1 infection of
microglia, as did MIP-1beta, which is a CCR5 ligand. Their results
suggest that both CCR3 and CCR5 promote efficient infection of the CNS
by HIV-1.

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

Dittmar MT, McKnight A, Simmons G, Clapham PR, Weiss RA, Simmonds P.
HIV-1 tropism and co-receptor use. (Scientific Correspondence
to Nature dated 2/7/97). Nature 385, 495 (1997).

Chemoattractant cytokines (chemokines) act during inflammation by
binding to and signalling through 7-transmembrane cell-surface
receptors. There has been much excitement over the discovery that
certain chemokine receptors, in cooperation with CD4 molecules on the
T-cell surface, also serve as entry portals for HIV. Various isolates of
HIV-1 use different chemokine co-receptors. This helps to explain why
some HIV isolates preferentially infect one or other cell type, a
property known as HIV tropism. Although almost all HIV isolates can
infect T-helper lymphocytes that have been activated to proliferate in
primary culture, only certain isolates can also infect macrophages,
whereas others infect immortalized T-cell lines. We show here that it is
oversimplistic to assume that chemokine co-receptor use accurately
reflects the cellular tropism of the virus.

. . .

It also apparent that macrophages express CXCR4, yet are not infected
by T-cell-line-adapted strains of HIV-1. We conclude that the ability
of a virus to use a co-receptor molecule does not necessarily confer
on that virus the ability to use that molecule on all cell types.
Post-translation modifications of co-receptors on macrophages may affect
their availability for infection by some HIV-1 strains but not others.

. . .

We have shown that the selective pressure on HIV-1 to immune escape from
neutralization can result in gaining the use of co-receptors.
Conversely, selection to use these new co-receptors, as the virus
colonizes various cell types in vivo during the progression to AIDS, may
result in escape from neutralizing antibodies.

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).

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

A friend of mind found out that her daughter’s best friend in
elementary school is HIV positive.  She is frantic.

What advice would you give to deal with the situation.  I heard
that there is no real danger in spreading the HIV virus through
normal social contact.  How would you safeguard your child while
at school and when they go visit the HIV-postive child?

ignore

The Internet’s most complete general store for your good health and
fitness. Browse our aisles or search our exhaustive data base by
category or keyword. Mother nature knows what’s best!  Visit
http://singlesalley.com/health.htm

Anyone out there know anything about chelation therapy.  I was told it’s a
medical procedure where the blood is rinsed? intravanously
with a solution of edta.  Correct or incorrect?   While this therapy is not
inexpensive, it’s supposed to be effective in removing cholestoral, other
plaques, heavy metals and chemical residues from the blood stream.  Sounds
good to me considering everything we ingest with all the processed foods and
chemicals used to grow our food.   I’m not any sort of health
service person. I’m in sales.

        The following showed up today on sci.med.aids.

In article <41…@sci.med.aids> SF AIDS Foundation
                                <b…@thecity.sfsu.edu> writes:

- Hide quoted text — Show quoted text -

>REPORT FROM THE FOURTH CONFERENCE ON
>RETROVIRUSES AND OPPORTUNISTIC INFECTIONS

>The following is an edited transcript of the BETA LIVE! conference
>call broadcast on January 26, 1997 from the Fourth Conference on
>Retroviruses and Opportunistic Infections held in Washington, DC.

>BAKER: Good afternoon everyone, and welcome to this special edition of
>BETA LIVE! I’m Ron Baker, Editor-in-Chief of BETA, the AIDS treatment
>magazine published by the non-profit San Francisco AIDS Foundation.
>    Today’s teleconference is brought to you live from the
>Sheraton Washington Hotel in Washington, DC, where over 2,500 AIDS
>researchers, clinicians and community activists have for the last 5
>days been attending the 4th Conference on Retroviruses and
>Opportunistic Infections, to hear about the latest results of recent
>research on AIDS.
>    This annual meeting is widely regarded as the single most
>important AIDS research conference in the world, and has featured an
>impressive roster of scientific presenters, including luminaries such
>as Dr. David Ho, recently named Time magazine’s "Man of the Year" for
>his contributions to advancing our understanding of the dynamics of
>HIV replication and how best to suppress the virus.

Ho! Ho! Ho!

>    With me today to review the conference presentations and to
>answer your questions are Dr. Trip Gulick of New York University;
>Dr. Cal Cohen, Director of the Community Research Initiative of New
>England; and Dr. Harvey Bartnof, a long-term member of the San
>Francisco AIDS Foundation’s Scientific Advisory Committee and a
>frequent contributor to BETA magazine.
>[....]
>GULICK: I think all of us continue to be amazed by the whole concept
>of viral dynamics — that is, how many viruses are produced and
>destroyed every day, and how many CD4 cells are infected on a daily
>basis. The first presentations at this meeting, by Dr. Alan Perelson
>from Los Alamos and Dr. David Ho from New York, reviewed the current
>thinking on viral dynamics, and the numbers are truly astonishing.

        They’re astonishing because they’re not real.

>    In a person in a steady state without treatment, on the order
>of a billion new viral particles may be produced every day, and the
>average life span of these viral particles is about 2 days. That means
>that the virus in an infected person’s system is turning over very
>fast.

        "There are no such things as slow retroviruses, just slow
retrovirologists." — Prof. Peter Duesberg

>[...]
>COHEN:…Another important issue — and ongoing debate — is the
>competence of the immune system. We have been seeing increases in the
>number of CD4 cells, but the mystery has always been whether immune
>cell competence is growing. What if your CD4 cell repertoire has been
>depleted? What if you’ve got only 40 CD4 cells/mm3? Can your body no
>longer fight certain infections?
>    We have started to get some information on this, although it
>is still quite early. It appears that the first wave of new CD4 cells
>may be just increases in numbers of the types of CD4 cells that you
>already have…

        It’s trafficking, Stupid!

-Giacomo
 Giacomo’s Cabaret, http://www.panix.com/~jscutero