From owner-immuno@hgmp.mrc.ac.uk  Wed Mar  1 08:10:14 2000
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From: Jamie Cunliffe <cunlij@my-deja.com>
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Subject: Re: "Danger" or "Alarm"?
Date: Wed, 01 Mar 2000 07:58:24 GMT
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In article <38AC84C2.C0BFCAC8@home.com>,
  D Forsdyke <forsdyke1@home.com> wrote:
> The word "danger" is currently popular among immunologists.
> However, "alarm" (Forsdyke, 1995) may be preferable, since it
> conveys the sense of a distinct call to action, whereas
> "danger" is an attribute which leads one to beware, or keep away.
>

Anyone following the "Danger" or "Alarm" or "The immune system is dead
…." Threads might find the following article illuminating. Here, I
guess, that I, too, have been guilty of skimming or reading with
blinkered eyes. Ibrahim et al in viewpoint paper in April 1995,
published in Immunology Today, 16:181-185+ outlined (essentially) the
mess/non-mess concept in language and a depth of understanding that
was, to my mind, spot on.

I would suggest that all contributors to these debates should read and
digest this article carefully. Personally, I wouldn't be tempted to
change a word in their article - either in respect of its "plain
English" or its conceptual content. It’s a pity that I had not
appreciated its content when devising the bibliography for my last
three articles. Perhaps I was just not conceptually ready for it.

Jamie

--
Waterside Health Centre, SO45 5WX, UK
Home pages
http://www.ndirect.co.uk/~greenprac/jamie/jamie%20main.htm


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From owner-immuno@hgmp.mrc.ac.uk  Wed Mar  1 17:35:54 2000
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From: Volker Blaschke <vblasch@gmx.de>
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Subject: TCR changes AFTER VDJ-recombination
Date: Wed, 01 Mar 2000 18:36:39 +0100
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We wonder if there could be changes within the TCR sequence AFTER the
recombination has taken place. Background is that we are trying to
identify malignant cells from a lymphoma, but we do find T-cell clones
with TCR sequences pretty similar to the presumedly "malignant
sequence".
So, do we have different cells indeed or might it be that these are
"subclones" of the malignant cell with ongoing TCR modifications? Would
these modifications be random, i.e. by "normal" mutagenesis, or are
post-rearrangement processes at work? Any references?

Thanks,

  Volker




From owner-immuno@hgmp.mrc.ac.uk  Wed Mar  1 18:10:30 2000
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From: Juliana <juliana77@my-deja.com>
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Subject: Courses
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Hi!
I'm a biology student looking for summer courses in Europe.
I'd be glad if anyone can help me.
Juliana

--
Education is not received.  It is achieved.


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From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  2 02:32:51 2000
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From: "Sara Valafar" <svalafar@cns.bu.edu>
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Subject: METMBS 2000 DEADLINE EXTENSION (MARCH 6)
Date: Wed, 1 Mar 2000 21:37:45 -0500
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The 2000 International Conference on Mathematics and Engineering
Techniques in Medicine and Biological Sciences
(METMBS'2000)
<http://www.cns.bu.edu/metmbs/>
(E-mail submissions are encouraged)

June 26 - 29, 2000
Monte Carlo Resort, Las Vegas, Nevada, USA
Call for Papers/Abstracts



Recent advances in computer technology have provided the tools and the
environment to study, analyze, and better understand complex systems. This
technological development has enabled researchers to collect and analyze
massive amounts of data to a scale previously not possible. The impact of
this technology is now being felt in the medical field and in the biological
sciences.   In recent years, research in interdisciplinary areas such as
Bioinformatics and computer assisted medical decision-making has
dramatically intensified.  METMBS'2000 aims to provide a platform for
researchers to present and discuss recent breakthroughs in this area.

The METMBS'2000 Conference will be held concurrently (i.e., same location
and dates) with the International Conference on Parallel and Distributed
Processing Techniques and Applications (PDPTA'2000), the International
Conference on Imaging Science, Systems, and Technology (CISST) and the
International Conference on Artificial Intelligence (IC-AI).

You are invited to submit a one-page abstract or a draft paper of about 4
pages, and/or a proposal to organize a technical session (see below for
submission information).  All accepted submissions will be published in the
conference proceedings.

THE NAMES OF TECHNICAL SESSION CHAIRS WILL APPEAR AS ASSOCIATE EDITORS ON
THE COVER OF THE CONFERENCE PROCEEDINGS.



SCOPE

Topics of interest include, but are not limited to, the following:

o Bioinformatics: This includes informatics techniques in genomics gene
sequencing, gene pattern discovery, gene pattern-function studies, and other
genomics related studies).

o Data mining in medicine and biological sciences.

o Pattern recognition in medicine and biological sciences.

o Signal processing in medicine and biological sciences (e.g. biomedical
signal processing, etc.)
o Image processing in medicine and biological sciences (e.g. biomedical
image processing, biomedical imaging, etc.)

o Medical decision-making.
o Medical Physics.
o Biomedical Engineering.
o Biomedical Electronics.
o Biosignal interpretation.
o Any application of computers in Medicine and biological sciences (protein
structure-function analysis, drug and protein design, molecular modeling and
simulation, etc.)
o Application of information technology in biomedicine (e.g. medical
database management, information retrieval and use of computers in
hospitals)
o Application of Computational Intelligence (artificial neural networks,
fuzzy logic, and evolutionary computing) in medicine and biological sciences
o Medical and bio-computing.
o Computer-based medical systems (automation in medicine, etc.)
o Recent history (1990-1999) of Mathematics and engineering techniques in
medicine and biological sciences, and what to expect during the next decade
(2000-2009); New horizons. Review articles)
o Other aspects and applications relating to technological advancements in
medicine and biological sciences.



SUBMISSION OF PAPERS

Prospective authors are invited to submit three copies of their one-page
abstract or draft paper (about 4 pages) to F. Valafar (address is given
below) by March 6, 2000.  E-mail and Fax submissions are also
acceptable.  The length of the Camera-Ready papers (if accepted) will be
limited to 7 pages.  Papers must not have been previously published or
currently submitted for publication elsewhere.

The abstract and the first page of the draft paper should include: title of
the paper, name, affiliation, postal address, E-mail address, telephone
number, and Fax number for each author.  The first page should also include
the name of the author who will be presenting the paper (if accepted) and a
maximum of 5 keywords.


PROPOSAL FOR ORGANIZING TECHNICAL SESSIONS

Each technical session will have at least 6 paper presentations.  The
session chairs will be responsible for all aspects of their sessions,
including soliciting papers, reviewing, selecting, ...

The names of session chairs will appear as Associate Editors in the
conference proceedings.  After the conference, some sessions will be
considered for publication in appropriate journals as Special Issues with
the session proposer as the Guest Editor of the journal.

Proposals to organize technical sessions should include the following
information: name and address (+ E-mail) of the proposer, title of session,
a 100-word description of the topic of the session, and a short description
on how the session will be advertised (in most cases, session proposers
solicit papers from colleagues and researchers whose work is known to the
session proposer).

Mail your proposal to F. Valafar (address is given below); E-mail
submissions are preferred.


EVALUATION PROCESS

Papers will be evaluated for originality, significance, clarity, and
soundness.  Two researchers in the topical area will referee each paper.
The Camera-Ready papers will be reviewed by one person.


PUBLICATION

The conference proceedings will be published by CSREA Press (ISBN).  The
proceedings will be available at the conference.  Some accepted papers will
also be considered for journal publication (soon after the conference).


ORGANIZERS/SPONSORS

A number of university faculty members and their staff, in cooperation with
the Monte Carlo Resort (Conference Division, Las Vegas), will be organizing
the conference.  The conference will be sponsored by Computer Science
Research, Education, & Applications Press (CSREA: USA Federal EIN #
58-2171953) in cooperation with research centers, international
associations, international research groups, and developers of
high-performance machines and systems.  The complete list of sponsors and
co-sponsors will be available at a later time.

The last conference's sponsors included: CSREA, the National Supercomputing
Center for Energy and the Environment - DOE, The International Association
for Mathematics and Computers in Simulation, The International Technology
Institute (ITI), The Java High Performance Computing research group, Korea
Information Processing Society, World Scientific and Engineering Society,
Sundance Digital Signal Processing Inc., the Computer Vision Research and
Applications Tech., and more.


LOCATION OF CONFERENCE

The conference will be held in the Monte Carlo Resort Hotel, Las Vegas,
Nevada, USA.  This is a mega hotel with excellent conference facilities and
over 3000 rooms.  The hotel is minutes from the Las Vegas airport with free
shuttles to and from the airport.  This hotel has many vacation and
recreational attractions, including: waterfalls, casino, spa, pools & kiddie
pools, sunning decks, Easy River water ride, wave pool with cascades,
lighted tennis courts, health spa (with workout equipment, whirlpool,
sauna,...), arcade virtual reality game rooms, nightly shows, snack bars, a
number of restaurants, shopping area, bars, ...  Many of these attractions
are open 24 hours a day and most are suitable for families and children.
The negotiated hotel's room rate for conference attendees is very reasonable
($79 + tax) per night (no extra charge for double occupancy) for the
duration of the conference.

The hotel is within walking distance from most other Las Vegas attractions
(major shopping areas, recreational destinations, fine dining and night
clubs, free street shows, and more).

For the benefit of our international colleagues: the state of Nevada
neighbors with the states of California, Oregon, Idaho, Utah, and Arizona.
Las Vegas is only a few driving hours away from other major cities and
attractions, including: Los Angeles, San Diego, Phoenix, the Grand Canyon,
and more.


EXHIBITION

An exhibit is planned for the duration of the conference.  We have reserved
20+ exhibit spaces.  Interested parties should contact F. Valafar (address
is given below).  All exhibitors will be considered to be the co-sponsors of
the conference.


IMPORTANT DATES

March 6, 2000 (Monday): One-page Abstracts or Draft papers (about 4
pages) due
April 3, 2000 (Monday):  Notification of acceptance
May 1, 2000 (Monday):  Camera-Ready papers & Preregistration due
June 26 - 29, 2000:  METMBS'2000 Conference

Proposals to organize technical sessions should be submitted as soon as
possible.  All accepted papers are expected to be presented at the
conference.


MEMBERS OF PROGRAM & ORGANIZING COMMITTEES

The Program Committee is currently being formed.  Those interested in
joining the Program Committee should e-mail F. Valafar (faramarz@cns.bu.edu
<mailto:faramarz@cns.bu.edu>) the following information: Name, affiliation
and position, complete mailing address, e-mail address, tel/fax numbers, a
short biography together with research interests.


OTHER INFORMATION

Last year PDPTA, CISST, and IC-AI had research contributions from over 44
countries (over 900 participants from all over the world.)  To make this a
more complete suite of conferences, we have added METMBS.  METMBS will also
have a strong international flavor and offers its participants an
introduction to a wide range of related interdisciplinary subjects through
the other three conferences.


CONFERENCE CONTACT:

          Faramarz Valafar
          Cognitive and Neural Systems
          Boston University
          677 Beacon Street
          Boston, MA 02215

          Tel: (617) 353-5134
          Fax: (617) 353-7755
          E-mail: Faramarz@cns.bu.edu <mailto:Faramarz@cns.bu.edu>

























From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  2 04:50:48 2000
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From: "W. Fred Shaw" <fredshaw@primenet.com>
X-Newsgroups: bionet.molbio.hiv,bionet.immunology
Subject: THE FAUCI FILES 3( 31): Israeli Diva's HAART Cocktail "Organ Failure"
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THE FAUCI FILES 3( 31): Israeli Diva's HAART Cocktail "Organ Failure"
March 1, 2000

While NIH/NIAID Director-Dictator Dr. Anthony "Mussolini" Fauci
continues to orchestrate his conspiracy of silence regarding
the lethality of the HIV/AIDS drug cocktail "standard of care" 
which he has personally orchestrated, the deaths keep climbing.

Here comes Ofra, the Israeli Diva with HIV who died of "organ
failure", purported to have been "related to AIDS". 

Oddly enough, AIDS has NEVER been associated with organ
failure, except for those who have used HAART and died of
organ failure as well (pick an organ: heart, liver, kidney,
adrenal, etc).

The Israeli media is promoting the notion:

                   "Ofra died of shame"

Unfortunately, HAART cocktail drugs don't kill through fatal
exacerbations of shame, they kill by massive metabolic 
disruption of every tissue and organ system of the body.

Meanwhile, Israeli health officials are correctly warning that 
there IS NO TREATMENT for HIV/AIDS and are calling for emphasis
on avoidance.

Whose will you, your patents and your corporate activists murder next, 
Dr. Fauci? Elton John?

Crooked Murdering Bastards!

W. Fred Shaw
Editor, THE FAUCI FILES
========================

Death of Israeli Pop Star Debated

By DINA KRAFT
.c The Associated Press

  
JERUSALEM (AP) - The death of a popular singer from AIDS, and her 
efforts to conceal her illness from the public, have sparked a furious 
public debate here about the right to privacy - and the stigma that some
here still attach to the illness. 

The refrain "Ofra died of shame" reverberated through Israel's 
newspapers and airwaves today. Haza's reported concealment and the 
widespread reaction to Monday's story about it in the Haaretz daily have
highlighted Israeli attitudes toward the disease. 

The 41-year-old diva died Wednesday of organ failure. Citing the 
singer's wish to maintain her privacy, doctors who treated her at Tel 
Aviv's Tel Hashomer Hospital refused to say what brought on her 
condition. 

However, Haaretz reported that she died of complications from AIDS. In 
an editorial, the paper said there was "no reason to demonize" the 
disease by keeping it a secret. The editorial called AIDS "a human 
disease like any other."

Doctors and family members maintained their silence, and there was no 
way to know how long Haza had been seeking treatment or how she might 
have contracted the disease. But Haza fans, politicians and others 
across Israel speculated today that if she had not feared negative 
publicity and had sought treatment sooner, she might not have died. 

"I think the shame, stigma, and lack of information are what killed 
her," said Tirza Ariel, widow of another popular Israeli singer. 

Fewer than 3,000 out of 6 million Israelis carry HIV, the virus that 
causes AIDS. Despite a recent Health Ministry campaign to increase 
public awareness, some Israelis still have misconceptions about the 
disease. 

AIDS activists lamented Haza's reported decision to keep her disease a 
secret, suggesting it reinforced the message that the disease is 
shameful. Others raised the prospect that in a more tolerant 
environment, Haza could have followed the example of someone like 
American basketball star Magic Johnson, who retired after his 1991 
disclosure that he is HIV-positive but has stayed in the public 
spotlight and become a campaigner for AIDS education. 

Some AIDS sufferers said friends and acquaintances surprised them by 
embracing them even after they had "outed" themselves. "Nobody ran 
away from me, nobody broke off the connection with me," said Avinoam 
Frumer. Others insisted there is a price for going public. 

Haza rose from the slums of Tel Aviv to become Israel's first 
international pop music star, blending ancient Yemenite Jewish 
devotional poetry with the sounds of 1980s techno music. 

Other papers and the electronic media said they also knew Haza had AIDS 
but did not run the story. Some lawmakers and other observers criticized
Haaretz for invading Haza's privacy. 

Haaretz's editorial cited widespread rumors about the cause of death and
Haza's status as a public figure in its decision to publish the report. 

"The attitude she bore toward the disease influences people, both 
healthy and infirm," Haaretz wrote. 

AP-NY-02-29-00 1128EST




From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  2 11:00:12 2000
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From: unknown@cam.ac.uk (Shared Mac)
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Subject: Boosting protein immunisation lowers Ab response
Date: Thu, 02 Mar 2000 12:06:43 +0100
Organization: University of Cambridge
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Hello to the denizens of bionet.immunology - I have a quick question.

Does anyone know if there are examples in the literature similar to the
following observation?

Following primary immunisation with a protein antigen (delivered using a
novel adjuvant) IgG Ab responses were observed that were significantly
higher than the response to Ag delivered in buffer.

Following a boost immunisation responses with adjuvant were even higher.

Following a second boost immunisation IgG Ab responses in the groups
receiving Ag in adjuvant had decreased compared to post-first boost and
were then not significantly different from the response in the groups
receving Ag in buffer.
Responses in the groups receiving buffer increased post-second boost so
this effect is not due to some problem with the Ag used in the second
boost.

Immunisations were s/c in mice.

Note also that at a low Ag dose Ab responses increased post-primary,
post-first boost and post-second boost for Ag delivered in adjuvant and
buffer.

Thanks for any pointers - please reply to the group.


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From: Michael Lang <mdlang@acs.ucalgary.ca>
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I'm putting together a lecture for 3rd year undergrads on the various
vaccines and strategies used. Does anyone know a good general reference
on vaccine development that may not be over their heads?



From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  2 17:23:42 2000
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Subject: Patient X, Walking Corpse (was Re: Need advice on bleeding and low platelets)
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Patient X, Walking Corpse (was Re: Need advice on bleeding and low 
platelets)

While it is not my intention to offend, abuse nor harass those 
who are ill, I have found that being nice in these public forums
doesn't get the point across when dealing with irrational systems 
of medical superstition and those who obey them as if they
were the religion du jour.

Since this post was published in this public forum, I post
this as a warning to all others, not necessarily the author
of the original post, whose email address has been omitted.

fred

On Thu, 02 Mar 2000 02:16:07 GMT, in
<38bdcb5d.41293435@news.mindspring.com> Patient X wrote
on misc.health.aids:

>I would appreciate any information on the problem of (apparenly) HIV
>induced low-platelet count. I'm currently on a hydroxyurea + DDI
>combo, which shouldn't be causing the problem

Excuse me? 

You are taking 2 of perhaps the most toxic drugs in the pharmacopeia
that are NOTORIOUS for suppression of the bone marrow and other
critically functional areas of the immune response. Anemia, platelet
anomalies, high cholesterol and heart disease aren't something to
trifle with, now are they?

H-E-L-L-O, wake up and smell the fucking coffee!

> and I've been in good, stable health for most of fourteen 
> years of being positive

Well you aren't anymore, now are you?

If you have been in "good, stable health for most of fourteen
years", then why the fuck are you using cancer chemo drugs?

Let this be a lesson for others who believe in excellent health
and everlasting life through superstitions about cancer chemotherapy
being "good" for viral diseases of immune suppression!

> and (my) other blood values ... are good:
>       vl undetectable, t4s in mid 400s, etc.

This certainly demonstrates the uselessness of these chemo-manipulated
lab values that have NOTHING to do with a better outlook for you since
you are using drugs which render these lab values invalid in the first
place.

Fact is, nearly everyone who is dropping dead has similar, if not
"better" lab values than yours (undoubtedly, including the dead
Israeli Diva who suffered "organ failure" on these cocktail poisons).

> I'm currently having a problem with ongoing posterior nasal bleeding,

You aren't the only one on these drugs to report this symptom. 

Others report intestinal bleeding too. Unfortunately, the blood
source is so high in the intestinal tract that the doctor's hemoccult
stool test can't pinpoint the source of the bleeding.

Have you considered eliminating the drugs from your diet for a couple
of weeks/months to see if your problems go away, or are you intent
on becoming another AIDS Martyr for the "betterment of science and
mankind" as so many other dead idiots have claimed for their suicidal
mission ?

> and although the docs have not yet been able to tell exactly 
> where it's coming from or what's causing it (I'm scheduled for a CAT scan)

The doctors are looking for a focal point, so believe me, they
will probably "invent one" from the CAT scan (you have no way to know
if they are bullshitting you or not, but they need to shut you up
long enough for your "life-saving" treatment to do its magic and 
kill you).

You also won't be the first to submit to recommendations for
nasal surgery. Someone I know in San Francisco had this same
problem, got the CAT scan and submitted to the surgery. He
almost bled to death on the operating table a couple of months
ago. What's worse, his sinus symptoms are much worse and he
has progressed to other complications require even more
medical interventions. He didn't heed the warnings. Neither
will you. You have both been brainwashed to worship the 
words of wisdom of the quacks in white coats.

> they're suggesting intravenous immune globulin treatment. 

This, of course, will be the doctor's final act of murder. Did you
realize that this is EXACTLY THE THING NOT TO DO, or do you intend
to get it over with as soon as possible?

Immune globulin "treatments" are nothing more than "food for virus".
The virus (and most viruses, not just HIV) will replicate like mad as
the Ig promotes B cell activation. If you don't get sick, go blind
or die from a viral breakthrough of one sort or another, it won't
be long before you get one of the new and improved lymphomas that
have only been seen in those using these cancer drugs.

So there you have it. Like it or not, you've been warned. Follow
your doctor's recommendations and you won't be the first to
find my words and warnings to be prophetic.

Good luck.

fred

[NOTE: For further details, search Deja.com for "THE FAUCI FILES"]

----
Full text of a walking corpse:

>I would appreciate any information on the problem of (apparenly) HIV
>induced low-platelet count. I'm currently on a hydroxyurea + DDI
>combo, which shouldn't be causing the problem, and all other blood
>values (at least the major ones I tend to pay attention to) are good:
>vl undetectable, t4s in mid 400s, etc., and I've been in good, stable
>health for most of fourteen years of being positive.  I'm currently
>having a problem with ongoing posterior nasal bleeding, and although
>the docs have not yet been able to tell exactly where it's coming from
>or what's causing it (I'm scheduled for a CAT scan), they're
>suggesting intravenous immune globulin treatment. Beyond the
>unpleasant side effects I've read about associated with IVIG, I'm
>wondering if there's anything less dramatic that might help? I just
>came across an article from AIDS Treatment News (4/4/97) that said
>that thiotic acid has been thought by some researchers to lower
>platelets, and I've been taking 500mg/day of this for several years.
>Has anyone else heard of this connection? Thanks in advance for any
>infomation!
>
>Patient X



From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  2 17:44:21 2000
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From: "Joe Chandler" <jchandler@mainebiotechnology.com>
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Here is a thought.
What was the time frame between the second two boosts?  If it was less than
three weeks, it is possible that the amount of circulating antigen-specific
Ig was high enough to form antigen-antibody complexes clearing most of your
immunogen out of the system.  This would results in a reducing the actual
amount of immunogen left to stimulate the immune system to quite a bit less
than you might expect.




From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  2 18:12:42 2000
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From: "W. Fred Shaw" <fredshaw@primenet.com>
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Subject: THE FAUCI FILES, 3( 32): Pantaleo: HAART Cocktail Trashes Critical CD8 Immunity
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THE FAUCI FILES, 3( 32): Pantaleo: HAART Cocktail Trashes Critical CD8
Immunity

March 2, 2000

As previously revealed by THE FAUCI FILES and now confirmed by
Pantaleo et al in the journal Blood (3/1/00, Soudeyns et al.),
who concludes that the HAART (HIV cocktail drugs) globally reduces
HIV-specific CD8 CTLs and suppresses HIV-1 replication in CD4+ T 
cells, but does not control HIV infection in tissue macrophages and 
dendritic cells.

In other words, HAART cocktail drugs are not "life savers" at
all. To the contrary, they are capable of causing the collapse
of life-critical immune protection directly.

Hence death-by-HAART.

Interestingly, Pantaleo once worked under Dr. Anthony "Mussolini"
Fauci at the NIH NIAID Institute, but left the little Mussolini
behind to return to conduct his research in Europe.

W. Fred Shaw, Editor, THE FAUCI FILES
---

The following contribution is from Billi Goldberg:

According to Schrager and D'Souza (1998), macrophages are reservoirs of 
HIV during all phases of disease progression.

According to Li et al. (1999), HIV-infected macrophages significantly 
increase their replicative capacity during advanced disease.

Since HAART eliminates cytotoxic/suppressive CD8 CTLs and cannot control
active HIV replication in infected macrophages (and/or dendritic cells),
there is a distinct possibility that disease progression will continue 
unabated during "successful" antiretroviral therapy.

As concerns the importance of these CD8 CTLs globally reduced by HAART, 
Soudeyns et al. (Pantaleo is senior author) state: "Acute or primary 
infection with human immunodeficiency virus type 1 (HIV-1) is 
characterized by transient high-level viremia, which decreases 
significantly upon the emergence of the host virus-specific immune 
response. Particularly effective in the control of primary as well as 
chronic HIV-1 viremia is the cellular immune response mediated by 
HIV-specific CD8+ cytotoxic T lymphocytes (CTLs).

The authors clearly admit that there is a problem: "Furthermore, 
similar to what occurs in chronic infection, the global reduction of 
CD8+ T-cell oligoclonality induced by HAART during primary infection is 
associated with a progressive reduction in the frequency of circulating 
HIV-specific CTL precursors and/or effectors. Therefore, it is 
conceivable that potentiation and long-term maintenance of a diversified
HIV-specific CTL repertoire during antiretroviral treatment may require 
the development of therapeutic vaccine strategies to achieve effective 
immune-mediated control of HIV replication."


Supporting article excerpts:

Dr. Guiseppe Pantaleo has reported that HAART does not control HIV 
replication in tissue macrophages and dendritic cells (Nature Medicine 
1997 May; 3(5): 483-486). He states: "A likely scenario is that 
antiviral therapy may effectively control active virus replication in 
the pool of high replicating virus cells (that is, CD4+ T cells), and 
not in the pool of low replicating virus cells, that is, tissue 
macrophages and/or dendritic cells, which account for the residual (<1%)
virus production. Therefore, the pool of low replicating virus cells 
seems to be mostly refractory to the potent antiviral drugs." 

In 1998, NIAID's Schrager and D'Souza stated: "Reservoirs of HIV-1 have 
been identified that represent major impediments to eradication. 
Conceptually, there are 2 types of sanctuaries for HIV-1, cellular and 
anatomical. Cellular sanctuaries may include latent CD4+ T cells 
containing integrated HIV-1 provirus; macrophages, which may express 
HIV-1 for prolonged periods; and follicular dendritic cells, which may 
hold infectious HIV-1 on their surfaces for indeterminate lengths of 
time."

The authors also state: "Macrophages may play important roles in 
abetting HIV-1 infection throughout the disease process, from soon after
initial mucosal exposure to the final stages. Human immunodeficiency 
virus 1 infection of macrophages can be productive but noncytopathic, 
permitting macrophages to serve as long-lived sources of HIV production.
Throughout the course of HIV infection, macrophages have been implicated
in carrying virus across the blood-brain barrier and establishing and 
maintaining HIV infection within the central nervous system (CNS), 
probably the most important anatomical HIV reservoir. During latter 
stages of HIV infection, when the CD4+ T-cell population is largely 
depleted, macrophages may be a key source of de novo HIV replication."

As concerns the importance of macrophages during disease progression, Li
et al. (1999) state: "However, this study also shows a marked and 
significant increase in replication as well as tropism for MDM 
[monocyte-derived macrophages] and monocytes by HIV-1 strains isolated 
from blood at the advanced stages compared with the early stages of HIV 
infection."

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

Soudeyns H, Campi G, Rizzardi GP, Lenge C, Demarest JF, Tambussi G, 
Lazzarin A, Kaufmann D, Casorati G, Corey L, Pantaleo G. Initiation of 
antiretroviral therapy during primary HIV-1 infection induces rapid 
stabilization of the T-cell receptor beta chain repertoire and reduces 
the level of T-cell oligoclonality. Blood 2000 Mar 1;95(5):1743-1751 

Laboratory of AIDS Immunopathogenesis, Division of Infectious Diseases, 
Department of Internal Medicine, Centre Hospitalier Universitaire 
Vaudois, Lausanne, Switzerland; Unit of Immunochemistry, DIBIT, and the 
Department of Infectious Diseases, San Raffaele Scientific Institute, 
Milan, Italy; Duke University Medical Center, Center for AIDS Research, 
Durham, NC; Fred Hutchinson Cancer Research Center, Seattle, WA 98105. 

E-mail: giuseppe.pantaleo@chuv.hospvd.ch

Abstract: Major T-cell receptor beta chain variable region 
(TCRBV) repertoire perturbations are temporally associated with the 
down-regulation of viremia during primary human immunodeficiency 
virus (HIV) infection and with oligoclonal expansion and clonal 
exhaustion of HIV-specific cytotoxic T lymphocytes (CTLs). To determine 
whether initiation of antiretroviral therapy (ART) or highly active 
antiretroviral therapy (HAART) during primary infection influences the 
dynamics of T-cell-mediated immune responses, the TCRBV repertoire was 
analyzed by semiquantitative polymerase chain reaction in serial blood 
samples obtained from 11 untreated and 11 ART-treated patients. 
Repertoire variations were evaluated longitudinally. Stabilization of 
the TCRBV repertoire was more consistently observed in treated as 
compared with untreated patients. Furthermore, the extent and the 
rapidity of stabilization were significantly different in treated versus
untreated patients. TCRBV repertoire stabilization was positively 
correlated with the slope of HIV viremia in the treated group, 
suggesting an association between repertoire stabilization and virologic
response to treatment. To test whether stabilization was associated with
variations in the clonal complexity of T-cell populations, T-cell 
receptor (TCR) heteroduplex mobility shift assays (HMAs) were performed 
on sequential samples from 4 HAART-treated subjects. Densitometric 
analysis of HMA profiles showed a reduction in the number of TCR 
clonotypes in most TCRBV families and a significant decrease in the 
total number of clonotypes following 7 months of HAART. Furthermore, a 
biphasic decline in HIV-specific but not heterologous CTL clones was 
observed. This indicates that ART leads to a global reduction of CD8(+) 
T-cell oligoclonality and significantly modulates the mobilization of 
HIV-specific CTL during primary infection. 

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

Schrager LK, D'Souza MP. Cellular and anatomical reservoirs of HIV-1 in 
patients receiving potent antiretroviral combination therapy.
JAMA 1998 Jul 1;280(1):67-71 

Epidemiology Branch, Division of AIDS, National Institute of Allergy and
Infectious Diseases, Bethesda, MD 20892, USA. LS14M@nih.gov 

Abstract: The eradication of human immunodeficiency virus 1 (HIV-1) from
infected persons is the ultimate goal of HIV therapeutic interventions. 
Great strides have been made in developing potent antiretroviral 
regimens that greatly suppress HIV-1 replication. Despite these 
therapeutic advances, major obstacles remain to eradicating HIV-1. 
Reservoirs of HIV-1 have been identified that represent major 
impediments to eradication. Conceptually, there are 2 types of 
sanctuaries for HIV-1, cellular and anatomical. Cellular sanctuaries may
include latent CD4+ T cells containing integrated HIV-1 provirus; 
macrophages, which may express HIV-1 for prolonged periods; and 
follicular dendritic cells, which may hold infectious HIV-1 on their 
surfaces for indeterminate lengths of time. The key anatomical reservoir
for HIV-1 appears to be the central nervous system. An understanding of 
the nature of HIV within these reservoirs is critical to devising 
strategies to hasten viral eradication. 

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

Li S, Juarez J, Alali M, Dwyer D, Collman R, Cunningham A, Naif HM. 
Persistent CCR5 utilization and enhanced macrophage tropism by primary 
blood human immunodeficiency virus type 1 isolates from advanced stages 
of disease and comparison to tissue-derived isolates. J Virol 1999 
Dec;73(12):9741-55 

Centre for Virus Research, Westmead Millennium Institute, National 
Centre for HIV Virology Research, Westmead, NSW 2145, Australia. 
Email: Hassann@westgate.wh.usyd.edu.au (Hassann Naif) 

Abstract: Viral phenotype, tropism, coreceptor usage, and envelope gene 
diversity were examined in blood isolates collected from 27 individuals 
at different stages of human immunodeficiency virus type 1 (HIV-1) 
disease and tissue derived isolates from 10 individuals with AIDS. The 
majority (89%) of blood and all tissue HIV-1 isolates from all stages of
infection were non-syncytium inducing and macrophage (M) tropic. 
Tropism and productive infection by HIV isolates in both monocytes and 
monocyte-derived macrophages (MDM) increased in advanced disease (HIV 
tropism for monocytes, 1 of 6 from categories I and II versus 11 of 21 
[P = 0.05] from category IV and II [CD4 < 250]; and high-level 
replication in MDM, 1 of 6 from categories I and II versus 16 of 21 from
categories IV and II [P = 0. 015]). There was a high level of 
replication of blood and tissue isolates in T lymphocytes without 
restriction at any stage. Overall, the level of replication in MDM was 
5- to 10-fold greater than in monocytes, with restriction in the latter 
occurring mainly at entry and later stages of replication. Only three 
blood isolates were identified as syncytium inducing, and all had a 
dualtropic phenotype. There was a significant increase of HIV envelope 
gene diversity, as shown by a heteroduplex mobility assay, in advanced 
disease; this may partly underlie the increase of HIV replication in 
MDM. Unlike blood isolates (even those from patients with advanced 
disease), tissue isolates displayed greater similarities (90%) in 
productive infection between MDM and monocytes. The majority (87%) of 
all isolates, including those from patients with advanced disease, used 
CCR5, and only 5 of 37 isolates showed expanded coreceptor usage. These 
results indicate that in the late stage of disease with increasing viral
load and diversity, CCR5 utilization and M-tropism persist in blood and 
tissue and the replicative ability in macrophages increases. This 
suggests that these characteristics are advantageous to HIV and are 
important to disease progression. 




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Subject: THE FAUCI FILES, 3( 33): NEJM Admits Illegal Falsifications, Fauci-Style
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THE FAUCI FILES, 3( 33): NEJM Admits Illegal Falsifications, Fauci-Style

March 2, 2000

While Byzantine politics has consumed the infectious disease
medical establishment under NIH/NIAID Direktor-Dictator
Dr. Anthony "Mussolini" Fauci, it appears that the takeover
of medical institutions by the pharmaceutical industry has
even reached the ivory tower of the esteemed New England
Journal of Medicine.

   "In an extraordinary apology to readers, the prestigious 
    The New England Journal of Medicine admitted violating 
    its financial conflict-of-interest policy 19 times over 
    the past 3 years in its selection of doctors to review 
    new drug treatments."

The New England Journal of Medicine has been added to the
"corporate sponsorship" list after it was busted for 
publishing articles by "researchers" who have been bought
and paid for by various pharmaceutical interests:

   "The internal review was prompted by a news report..."

Dr. Marcia Angell, NEJM editor in chief offers a false
apology in her too-little, too-late response:

    "It was carelessness on our part" 

and, the confession of Murder Inc.:

   "Angell said the stricter policy for review articles is 
    difficult to maintain because "there's so much connection 
    between academia and the private sector now." 

Naturally, one of the "careless" articles in question had to 
do with the HIV Haart Cocktail Drug hoax, which has been
entirely fueled by the phony hype surrounding similar
drug company exploits in the journal arena. This partial
list of falsified journal-article purveyors is a bit too 
familiar on the HIV/AIDS cocktail hype-circuit:

  "... (from) biotech companies to pharmaceutical giants like 
   Bristol-Myers Squibb, Merck & Co., Pharmacia & Upjohn, 
   and Wyeth-Ayerst."


Crooked Murdering Bastards!

W. Fred Shaw, Editor
====================

NEJM Apologizes for Conflicts of Interest 
 
Editor in Chief Faults Herself, Staff for 'Carelessness'  
 
By Linda A. Johnson 
 
Associated Press Writer 
 
Feb. 23, 2000 -- In an extraordinary apology to readers, the prestigious
The New England Journal of Medicine admitted violating its financial 
conflict-of-interest policy 19 times over the past 3 years in its 
selection of doctors to review new drug treatments. 
 
The Boston-based weekly journal, considered one of the world's premier 
medical publications, disclosed in Thursday's issue that it let doctors 
who had financial ties to the drug makers write the articles. 
 
"It was carelessness on our part," Dr. Marcia Angell, editor in chief 
since September, said in an interview. 
 
The internal review was prompted by a news report about one such 
violation last fall. It found 18 additional instances since January 
1997. 
 
The violations involve the journal's "Drug Therapy" feature, a series of
reviews of the latest drug treatments for particular illnesses. In each 
case, the journal failed to disqualify authors even though they had 
revealed their financial ties up front, Angell said. 
 
Angell said the journal solicits authors to write the reviews but is 
supposed to bar those that have directly or indirectly received "major 
research support" or payment as a consultant from companies that make 
drugs prominently discussed in those articles. 
 
The "Drug Therapy" series is overseen by an outside editor, Dr. Alistair
J.J. Wood, a pharmacology professor at Vanderbilt University in 
Nashville, Tenn. 
 
Angell said Wood disqualified authors who personally received 
significant research funding from the maker of drugs discussed 
prominently in an article but failed to disqualify authors whose 
institutions received such grants or authors who served as consultants 
to the drug companies. She said some in-house editors knew of the 
practice and overlooked it. 
 
She said she suspects there were violations before 1997, too, but the 
in-house review went back only 3 years. Wood has been editing the series
for about a decade. 
 
In a letter to readers, Angell apologized for the lapse and said steps 
have been taken to ensure against any recurrence. She said no action was
taken against Wood. He and a deputy editor who helps edit the series 
also signed the letter. 
 
The letter listed the 18 newly uncovered articles along with the drug 
makers, which ranged from little-known biotech companies to 
pharmaceutical giants like Bristol-Myers Squibb, Merck & Co., Pharmacia 
& Upjohn, and Wyeth-Ayerst. 
 
The journal regularly publishes original, unsolicited articles on 
clinical trials of particular drugs written by academic scientists who 
have received major research funding from a drug manufacturer involved. 
In those cases, the article notes those funding sources at the end. 
 
Angell said the stricter policy for review articles is difficult to 
maintain because "there's so much connection between academia and the 
private sector now." 

---



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From: Mike Clark <mrc7@cam.ac.uk>
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Subject: Re: Boosting protein immunisation lowers Ab response
Date: Fri, 3 Mar 2000 11:26:59 +0000
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In article <unknown-0203001206430001@acoff1.path.cam.ac.uk>, Shared Mac
<URL:mailto:unknown@cam.ac.uk> wrote:
> Hello to the denizens of bionet.immunology - I have a quick question.
> 
> Does anyone know if there are examples in the literature similar to the
> following observation?
> 
> Following primary immunisation with a protein antigen (delivered using a
> novel adjuvant) IgG Ab responses were observed that were significantly
> higher than the response to Ag delivered in buffer.
> 
> Following a boost immunisation responses with adjuvant were even higher.
> 
> Following a second boost immunisation IgG Ab responses in the groups
> receiving Ag in adjuvant had decreased compared to post-first boost and
> were then not significantly different from the response in the groups
> receving Ag in buffer.
> Responses in the groups receiving buffer increased post-second boost so
> this effect is not due to some problem with the Ag used in the second
> boost.
> 
> Immunisations were s/c in mice.
> 
> Note also that at a low Ag dose Ab responses increased post-primary,
> post-first boost and post-second boost for Ag delivered in adjuvant and
> buffer.
> 
> Thanks for any pointers - please reply to the group.
> 

You don't give details of timing or of the assay used for Ig. I can think
of two things that you should check for. 

[1] One is that you might be forcing the immune reponse to class switch to
a class or sub-class whihc you are not detecting in your assays.

[2] You might be forcing the system into a state of tolerance or
suppression for antibody responses to your antigen. This is more likely
with higher doses of antigen given more frequently.

Mike                            <URL:http://www.path.cam.ac.uk/~mrc7/>
-- 
 o/ \\    //            ||  ,_ o   M.R. Clark, PhD. Division of Immunology
<\__,\\  //   __o       || /  /\,  Cambridge University, Dept. Pathology
 ">    ||   _`\<,_    //  \\ \> |  Tennis Court Rd., Cambridge CB2 1QP
  `    ||  (_)/ (_)  //    \\ \_   Tel.+44 1223 333705  Fax.+44 1223 333875



From owner-immuno@hgmp.mrc.ac.uk  Fri Mar  3 13:21:36 2000
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From: "Mark Fowler" <mif@soton.ac.uk>
X-Newsgroups: bionet.immunology
Subject: Human Beta-Defensins.
Date: Fri, 3 Mar 2000 13:16:20 -0800
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Does anyone know where I can order HBD1 and HBD2 antibodies from,  someone
indicated that they are now available commercially.  Any help appreciated.

Mark Fowler
mif@soton.ac.uk





From owner-immuno@hgmp.mrc.ac.uk  Fri Mar  3 19:20:35 2000
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From: Nieves Gonzalez Ramon <ni.gonzalez.ramon@wxs.nl>
X-Newsgroups: bionet.immunology
Subject: Search on Medline
Date: Fri, 03 Mar 2000 20:27:32 +0100
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MEDLINE
Several interfaces allow the search on MEDLINE. Not willing to be
exhaustive I selected a sample of them:

1) Biomednet search interface.

http://www.biomednet.com/db/medline/advanced

This one offers a separate help window, independent from the search one
and giving brief but accurate info of the capabilities and a friendly
interface with menu choice of search fields.

a) Near operator for searching words in close proximity to each other.
Inside a phrase search, you can use the * to represent the possible
occurrence of intervening words. This is also known as ordered proximity
searching, as the words must still occur in the same order as they are
present in the phrase.
 e.g. 1 -Drosophila *1 homeotic- searches for the term "Drosophila"
followed by "homeotic" with no more than one intervening word. Items
retrieved include phrases such as "In Drosophila, most homeotic genes
are..." and "Drosophila homeotic genes are usually expressed...".
e.g. 2 -acetylation *5 histones- searches for "acetylation" followed by
"histones" with no more than 5 intervening words, and will match phrases

such as "acetylation of various Xenopus histones".

b) Wildcards Two symbols are available
* matches any number of characters including none. e.g. sul*ur matches
sulphur; sulfur. e.g. catheter* matches catheters; catheterisation;
catheterization; catheterise etc.
? matches exactly one character. e.g. sulf?nyl matches sulfonyl or
sulfinyl.
Using unnecessary wildcards may slow down response time. Consider using
stemming instead.

c) Stemming allows you to retrieve a group of words having the same word
root. For example, when stemming is switched on infection will also
match infect, infectious, infecting etc.
If the stemming checkbox is checked, stemming will be applied to all
query terms. If not, then + can be used after an individual word to
indicate that that word should be stemmed.
e.g. fluorescence+ and calcium produces around 50% more hits than
fluorescence and calcium
 Stemming is a faster alternative to wildcards, but, as with wildcards,
it cannot be used inside phrases.

d) Soundex matching
If you append the symbol $ to a search term, it will be matched using
soundex phonetic matching technology, to include similar sounding words.

e.g. stevenson$:au will match 'stevenson', 'stephenson' and 'stephens'
The soundex matching algorithm puts very loose constraints on what are
regarded as "similar" names, so it is most useful as an additional
constraint on an query rather than as a primary search mechanism itself.




2) The new version of PUBMED (launched on the web 4 months ago), with a
lot more of improved tools than the precedent one:

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?db=PubMed

 This new version of PubMed with pull-down menus that display
- Field limits, indexes
- HISTORY of search queries  and combination of them (typing each query
as #1, #2 and combining with the Boolean AND; OR ;NOT always in capital
letters).
- Hyperlinks to the FULL TEXT document. Depending on the publisher the
article will be of free access or on subscription.
- Allows "saving a search query" in the format of an URL, so that it can
be resent to get updates of your frequently used searches.

3) Internet Grateful Med (IGM) searches MEDLINE using the retrieval
engine of NLM's PubMed system.

 http://igm.nlm.nih.gov/

Additionally it contains other Databases:
MEDLINE, AIDSLINE, AIDSDRUGS, AIDSTRIALS, BIOETHICSLINE, ChemID,
DIRLINE, HealthSTAR, HISTLINE, HSRPROJ, OLDMEDLINE, POPLINE, SDILINE,
SPACELINE, TOXLINE.
- Also allows "saving a search query" in the format of an URL.

Regards






From owner-immuno@hgmp.mrc.ac.uk  Sat Mar  4 22:34:01 2000
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From: jwissmille@aol.com (JWissmille)
X-Newsgroups: bionet.immunology
Subject:  BERMUDA TRIANGLE of science-research dollars
Lines: 55
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[Note: Not only has CDC "misplaced" major funding for CFIDS/CFS research, but
admits to diverting funds from hanta virus--and now, in this segment, add Lyme
disease into the CDC, or BERMUDA TRIANGLE of science-research dollars.]

CDC SCANDAL:  Lively exchange at Senate hearing
                               by Roger Burns

WASHINGTON, Feb. 29 -- In contrast to a U.S. House of Representatives
hearing held earlier this month, today's hearing before a U.S. Senate
committee was lively, and was difficult for the official being
questioned, Dr. Jeffrey Koplan, Dircetor of the CDC.

Several questions were posed to Director Koplan about the CDC's
diversion of research funds and the adequacy of that agency's CFS
program, but Koplan's routine answers were not accepted by Senator
Herbert Reid (D-NV) and subcommittee chairman Senator Arlen Spector
(R-PA).  Sen. Reid expressed astonishment that a CDC employee had told
the Inspector-General that "It's a 'bigger crime' to follow Congress's
direction rather than spend money where science dictates", as reported
in the Washington Post and in other newspapers around the U.S. Reid said
that that was virtually spitting in the eye of Congress, and asked how
could the CDC keep such a person on its payroll.  Director Koplan said
he wasn't familiar with that employee and was unaware that such a
statement had been made, so he couldn't respond specifically, but the
quote given was antithetical to Koplan's own beliefs.  Sen. Reid also
said there were new reports that research funds for Lyme disease had
also been diverted.

Sen. Arlen Spector bore in to Dr. Koplan during his own question period.
Spector asked Koplan three times whether he had gotten more information
from the Inspector-General's office than just the official report. The
Senator further asked whether there were other diseases in addition to
hantavirus and CFS that were involved in the diversion of funds, to
which Koplan replied no. Spector also asked what disciplinary actions
the CDC had taken. At first Koplan responded that there had been a
re-assignment of one administrator. But under further questioning by
Spector, Koplan later said that the re-assignment had nothing to do with
a disciplinary action but was done only because that individual's
talents were more useful elsewhere.

At the end of the hearing, Spector asked Koplan whether he had
determined that false statements had ever been made about the CFS
program. At that point, HHS Secretary Shalala intervened and said that
the privacy laws which protect government employees prevent Director
Koplan from answering that question. After consulting with Secy. Shalala
in private, an apparently frustrated Senator Spector said he would defer
his question for the moment, but that it would ultimately be answered in
public, and if need be there would be an additional Senate hearing.

During today's hearing, Sen. Ted Stevens (R-AK) said that he felt this
entire issue was likely due to a misunderstanding and that no
misstatements were made intentionally by CDC staff. Sen. Stevens
outlined the need for improved coordination between the CDC and
Congress.



From owner-immuno@hgmp.mrc.ac.uk  Mon Mar  6 08:18:02 2000
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From: dickie <richard.horswill@creditlyonnais.co.uk>
Subject: glyconutritionals / how they may help with auto immune disease
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Nearly all disease is caused by Immune system dysfunction.
Due to stress, high levels of toxins in the air and water,
and nutritional deficiencies our immune systems are being
compromised. This could be reversable with the help of
Glyconutritionals. See website www.glycoscience.com for
more information.(richard.horswill@creditlyonnais.co.uk)


* Sent from AltaVista http://www.altavista.com Where you can also find related Web Pages, Images, Audios, Videos, News, and Shopping.  Smart is Beautiful


From owner-immuno@hgmp.mrc.ac.uk  Mon Mar  6 19:27:26 2000
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From: "W. Fred Shaw" <fredshaw@primenet.com>
X-Newsgroups: bionet.molbio.hiv,bionet.immunology
Subject: THE FAUCI FILES, 3( 35): Clerici: HIV Cocktails Shut Down Immune Response !
Date: Mon, 06 Mar 2000 11:27:08 -0800
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THE FAUCI FILES, 3( 35): Clerici: HIV Cocktails Shut Down Immune
Response !

May 6, 2000

Under the tutelage of NIH/NIAID Director Dr. Anthony "Mussolini" Fauci,
the budget-dictating bureaucrat behind HIV/AIDS research disaster
in America for the past two decades (the 80's, 90's and now the 00's),
let's take a close look at the "pinnacle" of Fauci's "leadership",
which we all know is the HIV cocktail "standard of care", otherwise
known as HAART (for Highly Active Anti-Retroviral Therapy, which
has recently lost it's "HA", and is now smugly called "ART", with
a tinge of grim humor).

Here are the golden words from the one who is one of Europe's 
greatest and most ethical HIV/AIDS researcher, Dr. Mario Clerici, who
has written the HA-ART epitaph in the January 28, 2000 edition
of the AIDS journal, where his team decisively compared the 
immunological profiles of the HAART-treated with the immunological 
profiles of antiretroviral-naive patients, both with undetectable
viremia:

   "HAART is associated with weaker HIV-specific and 
    -non-specific immune responses."

   "Our results show that immune responses are potent in 
    antiretroviral-naive but significantly reduced in 
    HAART-treated patients with undetectable viraemia 
    (< 500 copies/ml)."

   ". . . T-cell proliferation to HIV-specific and HIV-unrelated 
    antigens is potent in antiretroviral-naive but suppressed 
    in HAART-treated individuals; . . ."

As predicted from the outset of THE FAUCI FILES, it looks like 
the ART Hoax, stripped of its "HA", has reached the end of its 
Hype Cycle.

As to Fauci and his Corporate Activist minions assigned to this
newsgroup, this would be a good time to get out of town.

Crooked Murdering Bastards!

W. Fred Shaw
Editor, THE FAUCI FILES

By the way, the following article took eight (8) months to
be published (from submittal to publication) in a journal
which prides itself on the "fast track" publishing of
crucial treatment data. Now we understand the nature of the 
"fast track" litmus test for quick publication: the
article MUST NOT contradict a "standard of care" pharmaceutical 
product. 

Besides, one wouldn't think the AIDS journal wanted this
circulated prior to the recent San Francisco Pharmaceutical
HAART Hype-n-Schlock Conference.

Unlike the vast majority of the important AIDS journal articles,
good luck finding this one on the net as it is conspicuous
by its absence.

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

Clerici M,* Seminari E, Suter F, Castelli F, Pan A, Biasin M, Colombo F,
Trabattoni D, Maggiolo F, Carosi G, Maserti R (for the Master Group). 
Different immunologic profiles characterize HIV infection in highly 
active antiretroviral therapy-treated and antiretroviral-naive patients 
with undetectable viraemia. AIDS 2000 Jan 28; 14:109-116.

*Cattedra di Immunologia, Universita degli Studi di Milano, Via 
Venezian, 1, 20122 Milan, Italy. Tel: +390238210354; fax: +390238210350;
e-mail: mago@mailserver.unimi.it

Background: Suppression of human immunodeficiency virus (HIV) 
replication can be obtained in chronically infected individuals by 
highly active antiretroviral therapy (HAART) and can also be observed in
antiretroviral-naive patients. The immunological correlates of these two
situations were examined.

Design and methods: Cross-sectional study involving 32 HIV-infected 
patients with undetectable HIV plasma viraemia (< 500 copies/ml) and 
either antiretroviral-naive (n = 14) or undergoing HAART therapy with 
two nucleoside reverse transcriptase inhibitors (NRTI) plus one (n = 13)
or two (n = 5) protease inhibitors (PI). CD4 counts, disease duration, 
and CDC clinical stage were comparable between the two groups of 
individuals. Immune parameters (antigen- and mitogen-stimulated 
proliferation and cytokine production; cytokine mRNA; beta chemokine 
production; HIV coreceptors mRNA) were analysed in all patients.

Results: Results showed immune profiles to be profoundly different in 
antiretroviral-naive in comparison with HAART-treated patients. Thus: 
(1) T-cell proliferation to HIV-specific and HIV-unrelated antigens is 
potent in antiretroviral-naive but suppressed in HAART-treated 
individuals; (2) interleukin-(IL)2, IL-12 and interferon gamma 
(IFNgamma) production is robust in naive patients; and (3) a high 
CCR5/low CXCR4 pattern of HIV coreceptors-specific mRNA is observed in 
naive but not in HAART-treated patients. In contrast with these 
observations, no clear differences were detected when beta chemokine 
production by either peripheral blood mononuclear cells or purified CD8+
T-cells was analysed. Results from HAART-treated patients undergoing 
therapy with one PI and two NRTI or two PI and two NRTI were in very 
close agreement.

Conclusions: These data suggest that control over HIV replication can be
independently achieved by pharmacological or immunologic means. HAART is
associated with weaker HIV-specific and -non-specific immune responses.

---


From owner-immuno@hgmp.mrc.ac.uk  Mon Mar  6 21:00:19 2000
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From: rdara@uoguelph.ca (Rozita Dara)
X-Newsgroups: bionet.immunology
Subject: Post-doc position in autoimmunity
Date: 6 Mar 2000 20:50:03 GMT
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I am posting this announcement on behalf of Dr. Delovitch. Please address 
all correspondence directly to the following address:

Terry L. Delovitch, Ph.D. 
del@rri.on.ca 
Director, Autoimmunity/Diabetes Group 
The John P. Robarts Research Institute
1400 Western Road 
London, ON N6G 2V4
Canada  

Telephone: (519) 663-3972 
Facsimile: (519) 663-3847 

Postdoctoral Positions in Immunology of Autoimmune Diabetes Applications 
are invited for two postdoctoral positions available immediately to 
study: 1) the roles of cytokines, chemokines and their receptors in the 
immunoregulation of susceptibility to autoimmune 
diabetes in nonobese diabetic  (NOD) mice, and 2) the biochemistry of 
signaling and apoptosis in anergic NOD T cells.  These positions are 
available in conjunction with a JDF/MRC supported Diabetes Centre of
Excellence.  Highly motivated candidates should have a  recent Ph.D. or 
M.D./Ph.D. in immunology or related discipline, and be familiar with 
techniques in cellular/molecularimmunology, molecular biology, animal models 
of autoimmunity and gene transfer.  

Please email or fax CV, statement of research interests, and names and 
addresses of three references.










From owner-immuno@hgmp.mrc.ac.uk  Tue Mar  7 11:40:34 2000
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dickie <richard.horswill@creditlyonnais.co.uk> wrote in message
news:1ca4f2e8.09b62113@usw-ex0110-075.remarq.com...
> Nearly all disease is caused by Immune system dysfunction.


Where on earth did you get this notion?


> Due to stress, high levels of toxins in the air and water,
> and nutritional deficiencies our immune systems are being
> compromised. This could be reversable with the help of
> Glyconutritionals. See website www.glycoscience.com for
> more information.(richard.horswill@creditlyonnais.co.uk)
>

If toxins alone are the problem then that would be so easy to confirm ... .
It hasn't been.
Do it, then come back with your argument.



John H.


> * Sent from AltaVista http://www.altavista.com Where you can also find
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From owner-immuno@hgmp.mrc.ac.uk  Tue Mar  7 15:58:10 2000
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From: weigt@ita.fhg.de (Henning Weigt)
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Hello,

does anybody know about antibodys against human CCR7 (flow cytometry
use)?
I would appreciate any hints,

H. Weigt


From owner-immuno@hgmp.mrc.ac.uk  Tue Mar  7 20:49:46 2000
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From: jwissmille@aol.com (JWissmille)
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ou can still sign-up and get a room at the hotel!!  



******** 13th International  Conference on Lyme Disease and ****************
***************Other Tick-Borne Disorders ***********************
************* Clinical Management &  Research Update  *************

Jointly Sponsored by The College of Physicians  and Surgeons of Columbia
Universityand the Lyme Disease Foundation

Keynote Speakers: Attorney General Richard Blumenthal - Protecting the  Public
Health
 		          Willy Burgdorfer, PhD, MD (hon) - Discoverer of the pathogen
causing LD
			Senator Christopher Dodd - United States Senate - CT

March 25 & 26, 2000      Farmington Marriott, Farmington, CT

Place: Hartford Marriott, Farmington, CT   800-228-9290
   $79 single/double.  Reserve your room now. The hotel is expected to
sell-out! 
   Rate applies 3/23 - 3/27 - for those who want a side trip, maybe to Lyme,
CT!

Travel: Huntington Hay Travel  800-783-9783. Bradley is the closest airport
with shuttle service to the hotel. However, there is also a shuttle service
from  LaGuardia and Kennedy  airports (3 hr ride). 

****************** PROGRAM AGENDA *******

******** FRIDAY MARCH 24, 2000 
â€˘ Light Reception and Registration  7 - 10 pm

***** SATURDAY MARCH 25, 2000    

â€˘ Registration  7- 9am
â€˘ Program  8am - 5:30pm
â€˘ Reception 7-10pm

Presenters:
â€˘ Keynote:  Richard Blumenthal, Attorney General of Connecticut

â€˘ West Nile Virus:  Epicenter to epidemic and what to expect in 2000
		Tracey McNamara, DVM, Diplomate ACVP   National Wildlife Conservation / Bronx
Zoo	

â€˘ West Nile in Connecticut
		John Anderson, PhD   Connecticut Agricultural Experiment Station	

â€˘ Overview of human ehrlichioses and Rocky Mountain spotted fever in the US  
		Christopher Paddock, MD   Centers for Disease Control and Prevention

â€˘ Babesiosis  
		Peter Krause, MD   University of Connecticut School of Medicine

â€˘ Prevalence of infection in ticks submitted to the human test kit program of
the U.S. Army Center for Health Promotion and Preventive Medicine
	Ellen Stromdahl, MS  US Army Center for Health Promotion and Preventive
Medicine

â€˘ Analysis of Southern Borrelia
		Angela James, PhD   Centers for Disease Control and Prevention 

â€˘ Coinfections
		Louis Magnarelli, PhD   Connecticut Agricultural Experiment Station

â€˘ Preliminary in vitro and in vivo findings of hyperbaric oxygen treatment in
experimental Bb infection
		Charles Pavia, PhD   NY Medical College School of Medicine, NYCOM
Microbiology 				          and Immunodiagnostic
Laboratory of NYIT

â€˘ Immunity against host-adapted B. burgdorferi in the rabbit
		James Miller, PhD   UCLA School of Medicine

â€˘ Immunologic aspects of Vlse, a B. burgdorferi antigenic variation protein
		Steve Norris, PhD   University of Texas Medical School

â€˘ An immunodominant peptide of B. burgdorferi Vlse: Role in diagnosis &
pathogenesis
		Mario Philipp, PhD   Tulane University School of Medicine 

â€˘ Antibiotic treatment of Lyme borreliosis: A review of results with dogs
		Rheinhard Straubinger, DVM, PhD   Cornell University School of Veterinary
Medicine

â€˘ A Bb repetitive antigen that confers protection against experimental LD
		Jon Skare, PhD   Texas A & M University System Health Science Center

â€˘ Use of the borreliacidal assay in the serodiagnosis of Lyme disease
		Ronald Schell, PhD   University of Wisconsin School of Medicine

â€˘ Lyme neuroborreliosis - The role of  PCR and culture in the diagnosis and
in the confirmation of relapse after antibiotic treatment
		Jarmo Oksi, MD, PhD   Turku University Central Hospital, Department of
Medicine, Finland
					
â€˘ Laboratory Testing Panel
		Mark Golightly, MD   SUNY at Stony Brook School of Medicine
		Eli Mordechai, PhD   Medical Diagnostic Laboratories
		Ronald Schell, PhD   University of Wisconsin School of Medicine
		Jyotsna Shah, PhD   Igenex Laboratories
		Richard Tilton, PhD   BBI Clinicial Laboratories
		Steven Schutzer, MD   University of Medicine and Dentistry of New Jersey


                   SUNDAY MARCH 26, 2000 

Registration 7-8am (CME Sign-in)
Program 8AM - 5PM

Presenters:

â€˘ Keynote	Willy Burgdorfer, PhD, MD   National Institutes of Health

â€˘ Characterization of an immune evasion system in the Lyme disease
spirochetes
		Richard Marconi, PhD   Medical College of Virginia	

â€˘ Matrix metalloproteinases in Lyme disease
		George Perides, PhD   Beth Israel Deaconess Medical Center (Harvard)

â€˘ Interleukin-10 regulation during acute Lyme arthritis in dogs
		Reinhard Straubinger, DVM, PhD   Cornell University School of Veterinary
Medicine

â€˘ T-cell response
		Adriana Marques, MD   National Institutes of Health

â€˘ Protection against tick-transmitted disease in dogs vaccinated with a
multiantigenic vaccine 
		Alan Frey, PhD   New York University School of Medicine

â€˘ Update on the SKB OspA vaccine
		Dennis Parenti, MD   SmithKline Beecham Biologicals

â€˘ Atypical EM and acute Lyme disease
		Edwin Masters, MD   Regional Primary Care Physicians

â€˘ Neurologic Lyme disease in adults
		Patricia Coyle, MD   SUNY at Stony Brook School of Medicine

â€˘ Neurologic Lyme disease in children and adolescents
		Dorothy Pietrucha, MD, FAAP   Jersey Shore Medical Center, Meridan Health
System

â€˘ Cognitive deficits in children and the public health/educational
implications
		Marian Rissenberg, MD   Columbia University School of Medicine

â€˘ Neuroimaging in neuropsychiatric Lyme disease: Uses, abuses, and the future

		Brian Fallon, MD   Columbia University College of Physicians & Surgeons

â€˘ Pharmacologic properties of antibiotics and their relevence to LD
		Sam Donta, MD   Boston University School of Medicine

â€˘ Treatment Roundtable 
		Joseph Burrascano, MD   Southampton Hospital
		Sam Donta, MD   Boston University School of Medicine
		Lesley Fein, MD   Morristown Memorial Hospital
		Kenneth Liegner, MD   Westchester Medical Center
		Dorothy Pietrucha, MD   Cornell/NYHospital, Jersey Shore Medical Center 

 â€˘â€˘â€˘â€˘Â Target Audience
This conference is designed for clinical professionals (including but not
limited to Primary Care Physicians, Nurse Practitioners, Physician Assistants,
Public Health Officers, Researchers and Veterinarians) and other health
professionals (medical directors, risk managers) who wish to enhance their
knowledge of Lyme disease and other tick-borne disorders.  

â€˘â€˘â€˘Â Program Committee
James Miller, PhD  UCLA School of Medicine
Sam Donta, MD Boston University School of Medicine
Brian Fallon, MD Columbia University College of Physicians & Surgeons
Ed Bosler, PhD  Stonybrook School of Medicine
Julie Rawlings, MPH  Texas Department of Health
Charles Pavia, PhD  New York Medical College
Ronald Schell, PhD  University of Wisconsin School of Medicine

â€˘â€˘â€˘   Accreditation
This activity has been planned and implemented in accordance with the Essential
Areas and Policies of the Accreditation Council for Continuing Medical
Education (ACCME) through the joint sponsorship of the  College of Physicians &
Surgeons of Columbia University and the Lyme Disease Foundation.
The  College of Physicians & Surgeons of Columbia University is accredited by
the Accreditation Council for Continuing Medical Education (ACCME) to sponsor
continuing medical education for physicians and takes responsibility for the
content, quality and scientific integrity of this CME activity. 
The  College of Physicians & Surgeons  designates this educational activity for
a maximum of 15 hours in Category 1 credit towards the AMA Physicianâ€™s
Recognition Award. Each physician should claim only those hours of credit that
he/she actually spent in the educational activity.

â€˘â€˘â€˘â€˘Â Conference Goals
a. Recognize the complex nature of Borrelia burgdorferi in both in terms of its
antigenic variability and the host response to infection;
b. Understand the rationale for different treatment approaches to Lyme Disease
in animals and humans;
c. Clarification of the role of the multiple diagnostic tests for Lyme disease;
d. Understanding better the presentations of neurologic Lyme disease in
children and adults, including the role of neuropsychological testing and
neuroimaging;
e. Understanding the epidemiology, clinical phenomenology, and diagnostic
methods for detecting other vector-borne diseases, such as babesiosis,
ehrlichiosis, Rocky Mountain spotted fever, and West Nile virus; 
f. Understanding the latest research regarding Lyme vaccines.

Disclosure
Before the program, all faculty will disclose the existence of any financial
interest and/or other relationship(s) (e.g. employee, consultant, speakerâ€™s
bureau, grant recipient, research support, stock ownership or any other special
relationship) they might have with a.) the manfacturer(s) of any commercial
product(s) to be discussed during their presentation and/or b.) any commercial
contributor to this activity.  When unlabeled uses are discussed, these will
also be indicated.

***************** REGISTRATION  *******************
Mail to:  Lyme Disease Foundation, 1 Financial Plaza, Hartford, CT 06103
860-525-2000   Fax 860-525-8425  Hotline 800-886-LYME
Lymefnd@aol.com     www.Lyme.org

Fee includes: Attendance at scientific sessions, book of proceedings, lunch and
breaks on both days, and receptions Friday (3/24) and Saturday (3/25) night.
__  $275  February 16 to March 21 
__  $325  March 22 to on-site
__  $160  Poster Presenters - Posters still being accepted as of 3/7/00.  
Contact us for forms ; Graduate Students  - w/University validation letter. 
__  $60   Reception Only 
__  $20   CME Certificate 

***** Check Enclosed  - Make checks payable to â€śLyme Disease Foundationâ€ť 
**** Credit Card Charge
       __ Mastercard          __ Visa         __ American Express
Card #_______________________________ Exp. ______ 
Signature________________________________________
Total Payment Enclosed: $ ____________
               Full payment must accompany registration form. 

** REGISTRANT #1
   Name:
   Title/Position:
   Degree(s):
   Institution:
   Mailing Address:
   City:                           State               Zip
   Phone:
   fax; 
   email:
    ___ CMEâ€™s ___CME Certificate ($20 extra)  
   Signature 

** REGISTRANT #2 
   Name:
   Title/Position:
   Degree(s):
   Institution:
   Mailing Address:
   City:                           State               Zip
   Phone:
   fax; 
   email:
    ___ CMEâ€™s ___CME Certificate ($20 extra)  
   Signature 






From owner-immuno@hgmp.mrc.ac.uk  Wed Mar  8 05:14:15 2000
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CD40 Protein is available from Ancell Corp. in Minnesota. Check 
their website at: www.ancell.com

-- 
Linscott's Directory of Immunological & Biological Reagents
815 Whitney Way, Petaluma, CA  94954
phone: 707-763-7098  fax: 707-763-8372
URL = www.linscottsdirectory.com


From owner-immuno@hgmp.mrc.ac.uk  Wed Mar  8 05:18:25 2000
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Probably the best sources of lectins are the following companies:
E-Y Laboratories
ICN Biomedicals
Sigma Chemical Co.

-- 
Linscott's Directory of Immunological & Biological Reagents
815 Whitney Way, Petaluma, CA  94954
phone: 707-763-7098  fax: 707-763-8372
URL = www.linscottsdirectory.com


From owner-immuno@hgmp.mrc.ac.uk  Wed Mar  8 09:22:40 2000
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Subject: Re: glyconutritionals / how they may help with auto immune disease
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I actually think that nutrition is the key. Our modern diets do
not completely sustain the body`s needs, hence the increase in
immune system dysfunction.(Thats the theory anyway) That is why
I take a glyconutritional supplement.See www.glycoscience.com


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From owner-immuno@hgmp.mrc.ac.uk  Wed Mar  8 16:19:43 2000
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From: Agnes Doumas <adoumas@dplanet.ch>
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Subject: I'm not a specialist...
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Could anyone help me in answering to the following questions:
 
Is it possible to raise antibodies against molecules such as Colchicine
(some kind of molecules based on about
25-35 C, 35-40 H, 5-7 O, and possibly F, Na, N... and including about
3-4 cycles)? What may be the chances?
 
 What are the types of molecules (except proteins and carbohydrates)that
are antigenic??

Thanks a lot for your answer!

ADo


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Dear collegues,

I´m looking for the human IL-2 dependent cell lines NK-92 and Kit225-K6. I
would appreciate if someone form Germany or Europe could send me a few ml
of these cells by mail.

Thanks in advance,


Holger Fehr

-------------------------

Dr. Holger Fehr
Inst. Physiological Chemistry II
University of Wuerzburg
Biocentre
Am Hubland 
D-97074 Wuerzburg
Germany 
---


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From: "Graham Shepherd" <muhero@globalnet.co.uk>
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Subject: Re: glyconutritionals / how they may help with auto immune disease
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dickie <richard.horswillNOriSPAM@creditlyonnais.co.uk.invalid> wrote in
message news:0cbe8fc0.d17a6ff8@usw-ex0103-023.remarq.com...
> I actually think that nutrition is the key. Our modern diets do
> not completely sustain the body`s needs, hence the increase in
> immune system dysfunction.(Thats the theory anyway) That is why
> I take a glyconutritional supplement.See www.glycoscience.com
>

That's not a theory, it's a belief. If you're happy with it, fine. But
believing the world is flat doesn't make it so.

GS




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From: "W. Fred Shaw" <fredshaw@primenet.com>
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Subject: THE FAUCI FILES, 3( 38): Anti-Retroviral Therapy (ART) Corporate Revisionism, Point-Counterpoint
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THE FAUCI FILES, 3( 38): Anti-Retroviral Therapy (ART) Corporate
Revisionism, Point-Counterpoint

March 8, 2000

I am providing the following point-counterpoint analysis 
in response to Project Inform San Francisco's 
"Founding Director", Martin Delaney. As the leader of
the pharmaceutical Corporate "Treatment Activists", 
Mr. Delaney receives pharmaceutical funding and his 
periodic product editorial defenses, publications 
and lobbying efforts are obviously on behalf of the 
pharmaceutical industry.

Although Mr. Delaney and his organization claim to
represent a patient "constituency", it is worth noting
that Mr. Delaney's corporate commentary doesn't seriously
consider the negative health implications of ART 
for his purported constituency: the HIV/AIDS patient
(in fact, Mr. Delaney himself is HIV-negative).

Finally, it is also worth noting that Mr. Delaney's
Project Inform Board of Directors includes such luminaries
as Aaron Diamond's Dr. David Ho and Dr. Robert Gallo,
as well as others who have disclosed significant financial
conflicts of interest with the pharmaceutical industry.

W. Fred Shaw, Editor
THE FAUCI FILES
===============

Return-Path: <mary@aegis.org>
Message-Id:  <4.3.2.20000306230000.00dd4e10@127.0.0.1>
Date:        Mon, 06 Mar 2000 23:05:37 +0000
To:          "aids" <webmaster@aegis.com>
From:        "Sr. Mary Elizabeth, OSM" <mary@aegis.org>
Subject:     [AEGiS] Response commentary to Clerici article 
             posted March 5, 2000

>Submitted by Martin Delaney
>Project Inform
>--------------
>
>There is nothing either new or unusual about this.

Nothing could be further from the truth. 

> It is a phenomenon that has been reported and discussed repeatedly 
> among immunologists at meetings both privately and publicly. It does 
> not suggest a fault of therapy, but rather the success of it.

Again, nothing could be further from the truth.

FACT: this is the first time that a major scientist has separated 
those treated with antivirals from those who were antiviral
naive for the purpose of measuring, comparing and contrasting the 
immunological parameters of the ART-treated versus the ART-naive
(those who have never received ART treatment).

Although the Clerici et al article in the journal AIDS (1/28/00) 
was NOT an evaluation of the clinical relevancy or usefulness 
of ART therapy (personal communication), no true scientist of 
Clerici's impartial and ethical stature should ever participate 
in product research evaluations and recommendations.

Therefore, while remaining impartial as to the clinical usefulness
or validity of ART, Dr. Clerici et al nonetheless reports
objective findings that are rather startling and unambiguous:

  "Our results show that immune responses are potent in 
   antiretroviral-naive but significantly reduced in
   HAART-treated patients with undetectable viraemia (< 500 copies/ml)."

  "T-cell proliferation to HIV-specific and HIV-unrelated antigens is 
   potent in antiretroviral-naive but suppressed in HAART-treated 
   individuals; . . ."

  "Results: Results showed immune profiles to be profoundly different in
   antiretroviral-naive in comparison with HAART-treated patients. Thus:
     
     (1) T-cell proliferation to HIV-specific and HIV-unrelated antigens
         is potent in antiretroviral-naive but suppressed in 
         HAART-treated individuals; 

     (2) interleukin-(IL)2, IL-12 and interferon gamma (IFNgamma) 
         production is robust in naive patients; and 

     (3) a high CCR5/low CXCR4 pattern of HIV coreceptors-specific mRNA 
         is observed in naive but not in HAART-treated patients.

> It does not suggest a fault of therapy, but rather the success of it.

If one views immune suppression as a proper goal for a fatal
pathogenic disease with a symptomatic hallmark of immune suppression,
then ART is certainly a resounding, albeit deadly, "success".

> This reduction in the HIV specific immune response is a direct result
> of the reduction in viral replication as a result of therapy.

Nothing could be further from the truth. Immune suppression
by these ART drug therapies occurs independently of the
individual's viral load. Thus, the suppression of the entire 
immune response -- not merely the HIV-specific response -- 
is a primary and direct effect of these drugs rather than 
a downstream effect of viral reduction.

The reduction of ALL immune responses, including such things
as the candida and flu antigens (Clerici et al, AIDS, 1/28/00), 
were only observed in those using the ART drugs:

1. Treatment "failures" who use these ART drugs, achieve non-detectable
   viral loads but later experience viral rebound do NOT experience a 
   concomitant "rebound" in their HIV-specific immune response, as Mr. 
   Delaney suggests.

2. Treatment "failures" who use these ART drugs and do NOT achieve
   significant viral load reduction, will nonetheless suffer the same 
   ART-induced immune suppression as those who do achieve non-detectable
   viral loads. 

3. Treatment "naives" who never use these drugs and have low and 
   undetectable viral loads do NOT experience the loss of immune 
   responses -- HIV-specific or otherwise -- that are reported
   only for the ART-treated.

Mr. Delaney merely parrots the superstition promulgated by the
pharmaceutical industry that claims that these drugs are specific to
the HIV virus. Nothing could be further from the truth.

> What maintains that response in naive (untreated) patients 
> is the constant stimulation of the immune system by viral replication.

This focus on the HIV-specificity subset of the immune response
merely detracts from the immune response as a whole, which is clearly
being destroyed by the ART drugs.

FACT: The Clerici article clearly makes the unambiguous distinction 
between the HIV-specific and other immune responses:

   "T-cell proliferation to HIV-specific and HIV-unrelated antigens 
    is potent in antiretroviral-naive but suppressed in HAART-treated 
    individuals; . . ."

The reduction of HIV viral load does NOT account for the loss of
immune responses to other antigens, which were "defective"
ONLY in the ART-treated, such as the candida- and flu-specific
antigens.

> Once that is suppressed a few logs, the immune system no longer
> sees much HIV and therefore stops attempting to respond.

Rubbish. The immune systems of the ART-naive don't "stop
attempting to respond" when their viral load is "suppressed
a few logs" in the absence of these drugs. Further, as stated
above, those who use ART and do NOT achieve reductions in
viral load will nonetheless experience the same decline in
immune responsiveness as those who do achieve non-detectable
reductions in the HIV viral load.

>In people treated since the earliest stages of infection, it appears
>that this HIV specific immune response is sometimes preserved, or at
>least the capacity for making it.

At best, this statement is a very poor advertisement for using
these immune-destroying drugs for a disease of declining
immunity.

Clearly, ART suppresses ALL immune responses directly, NOT as a
secondary effect of reducing the HIV viral load. Terms such as 
"sometimes preserved" and "capacity for making" are, in this case, 
simple artifacts of Delaney's distance from the science.

> In some of the STI (therapy interruption) research, this response
> has been triggered after people go off therapy for a while.

Dr. Clerici et al detailed the overbroad suppression of
the immune response in the ART treated while the immune responses
of the ART-naive remain intact. Mr. Delaney offers no explanation 
for the intact immune responses of the treatment naive with 
low and undetectable viral load. 

Are the immune responses (HIV-specific and otherwise) of the 
treatment-naive suppressed in the presence of viral control? 
Of course not. Do the ART-naive retain their immunological
response to the flu and candida antigen? Yes.

Are the immune responses (HIV-specific and otherwise) of the 
ART treated suppressed in the presence of viral control? Yes. 
Do the ART-treated retain their immunological response to the 
flu and candida antigens? No.

(see references below) 

> Although the numbers are still relatively small, there is some 
> small, there is some indication that repeated cycles of on/off therapy
> can strengthen the natural immune response.

The claim that a "small number" or a "small indication" of
ART users who engage in "on/off therapy" will "strengthen the 
natural immune response" is made in the absence of comparative 
data involving the treatment naive. Such unscientific studies
in the absence of placebos or comparative data involving
those who are NEVER ART-treated have clearly dominated the
approval and recommendation process for these ART drug 
therapies for the past 13 years -- almost to the exclusion 
of anything else.

In fact, in this "small number" of those who use ART without
measurable loss of immune responses, Occam's Razor could favor only 
one conclusion: these individuals would have done the same or 
better had they not used the ART drugs in the first place.

> More than a dozen people are currently being studied who underwent 
> anywhere from one to three cycles of treatment interruption and 
> who now maintain undetectable viral load without further help from  
> antiviral drugs.

Absent a comparative group of treatment-naive, Delaney's "dozen people"
anecdote may be interesting, but offers little or nothing
in terms of scientific evidence, especially when we aren't 
being advised of the pre-treatment viral load of these
purported individuals.

To rely on such pie-in-the-sky studies after 13 years of these
toxic and dangerous pharmaceuticals as the "standard of care"
is as irresponsible as it is intentional in the deaths of those
who die as a direct result of using these drugs.

>It has also been noted that each time a treatment interruption cycle is
>used, it typically takes longer for viral load to become detectable
>again.

Obviously this observation could better be explained as an 
artifact of the cycles of ART-induced immune suppression, 
together with the dynamics of multi-drug resistance (MDR). 

>Until recently, this phenomenon had only been seen in people treated
>since primary infection. A new report was released at the VII
>International Retrovirus Conference which showed a similar outcome in a
>small number of chronically infected patients as well.

For the most part, the conference reports upon which Delaney relies
are little more than publicity stunts and appeals for drug company
research funding (they were never intended for peer-reviewed 
journal publication). The reliance on non-peer-reviewed and 
journal-unpublished anecdotal data from pharmaceutical conferences 
is not only typical of poor salesmanship, but clearly demonstrates the 
scientific and clinical bankruptcy of ART itself.

>Taken together, it might be suggested that the way to avoid loss of the
>HIV-specific response requires two steps.

Once again, the "HIV-specific" sales tactic avoids the most important 
issue: the overbroad loss of ALL immune responses, not merely those
related to HIV-specificity.

> First, it seems clear that the best chances for maintaining the 
> capacity to mount that response is to treat people early 

Mr. Delaney has struggled to make these issues anything but clear.

To use ART immune-suppressing drugs to suppress the immunological
control which, in the absence of these drugs, delays the 
onset of symptomatic disease for a decade or longer, could only 
portend a grim outlook for the patient.

Further, Mr. Delaney's lack of scientific candor is as abysmal as his
lack of scientific evidence to sustain the continued use of
the ART 13-year standard-of-care, which, as we can all plainly
see, has never been "standardized" nor has it offered "care"
in terms of preserving the competence of the innate immune response.

If a therapy for a disease of immune suppression fails to
protect and preserve the immune health of the patient, but
rather does harm to these life-critical protective processes,
then what good is it?

> (this, however, must be balanced against the earlier
> risks of side effects).

The early onset of "side effects" from ART "early use" is as
obvious as it is destructive of every tissue and organ system
of the body. Unfortunately, these "hit hard and hit early"
patients will most likely die of organ, vascular and/or a
variety of immune failures prior to the time they would be 
expected to develop AIDS. This can be seen in the preponderance
of obituary reports which reveal "sudden death" which is often
characterized as "not AIDS related". The very recent death 
of the Israeli Diva who died of "organ failure" offers a
case in point and begs an answer to the question that
arose after the approval of these ART drugs: what 
causes "organ failure" in those with HIV infection, if 
not the ART drugs?

> Secondly, preliminary data suggest that treatment needs to be 
> interrupted periodically to permit the virus to be
> "reintroduced" to the immune system periodically.

It was only a few short years ago that Mr. Delaney authored
an editorial in the Project Inform "PI Perspective", in
which he emphasized the life-critical importance of NEVER
missing a single dose of the ART regimen. Mr. Delaney's
precise words began with the alarmist admonition:

    "You have one chance to get it right ..."

Today, Martin Delaney is promoting the ART product line
with quite a different spin that underscores the
"benefit" of ART that is "interrupted periodically".

What corporate product spin will Delaney offer us a year
or two from now?

Further, as one of the favored corporate spins, the "potential
-but-not-quite-a-cure" sales tactic is not without precedent
(e.g. the implications for Delaney's latest spin on
the ART treatment theory: "permit the virus to be 'reintroduced' ... "),
as this was the original impetus for these drugs gaining
initial FDA approval in the first place. Aaron Diamond's 
Dr. David Ho (on Mr. Delaney's Project Inform Board of Directors)
played no small role in purveying this false treatment
claim in his 1996 claim for the ART "1 year cure", which
he later clarified as his "mathematical cure". Dr. Ho's 
superstitious claims have yet to materialize, however here 
they rematerialize in Delaney's own words that unambiguously 
imply that HIV virus "leaves the body" as a result of using
the ART drugs. Mr. Delaney, however, takes the superstition
to the next marketing level with the implication that
when the drugs are stopped, the virus will mysteriously be 
"reintroduced", as if that is something that is good, healthy
and desirable. Such is the nature of medical hucksterism.


To conclude this point-counterpoint analysis, it is essential
to re-examine the scientific rationale for Dr. Fauci's
ART "standard of care", which originally focused on
these drugs as potent weapons that would facilitate
the reconstitution of the immune response through the
decrease of the viral load, which, in turn, would
result in increases of the CD4+ T-cell count. (Interestingly, 
under NIAID Director Dr. Anthony Fauci's tutelage, Mr.
Delaney is listed by NIH/NIAID as a contributor to the development
of the ART "Standard of Care" recommendations, despite his
lack of medical or scientific credentials).

While Clerici et al, Pantaleo et al and others have recently
revealed that "HAART (ART) does not necessarily augment the 
immune response", then this can no longer be a rationale
for using HAART when the immune responses required
to control opportunistic infections and neoplasms are not 
only NOT being augmented, but to the contrary -- these
immune responses (e.g. including the flu and candida
antigens, Clerici et al, AIDS, 1/28/00) are being directly 
suppressed and harmed by ART!

Finally, the proposition that immunomodulators are needed
to "augment" ART is implicitly flawed when one considers
that these immunomodulators are merely needed to compensate
for the immune harm that is done by the first treatment (ART).

The treatment question remaining is obvious: can immunomodulators
even begin to compensate for the immune destruction done by ART,
and if so, wouldn't they be even more valuable in the control
of the HIV virus when they are used alone and in
the absence of ART, rather than as a medical intervention
that chases the harm done by ART, a therapy that can no
longer claim a valid "immune augmenting" rationale?

Isn't it rather revealing that these are the questions that
Mr. Delaney, Dr. Fauci, Dr. Ho and their various corporate
minions and sponsors are NOT bothering to ask for the betterment 
of what Delaney purports to be his "patient constituency"?

W. Fred Shaw, Editor
THE FAUCI FILES

========

The following articles by elite scientists, including Nobelist Rolf 
Zinkernagel, provide conclusive evidence that HAART: 

  (1) increases blood CD4 T-cells -- not by creating NEW CD4 T-cells,
      but rather by inducing the redistribution of the CD4 cells
      that are ALREADY present in the lymphoid tissues (thus,
      the lab CD4 measure becomes a superstitious treatment
      artifact of no true value).
  (2) increases CD4 T-cells which are suppressors, 
  (3) suppresses immune responses, 
  (4) suppresses cytokine production, and 
  (5) virological failure does not involve drug-resistant HIV-1 
      mutations:
 
(1) Bucy RP, Hockett RD, Derdeyn CA, Saag MS, Squires K, Sillers M, 
Mitsuyasu RT, Kilby JM. Initial increase in blood CD4(+) lymphocytes 
after HIV antiretroviral therapy reflects redistribution from lymphoid 
tissues. J Clin Invest 1999 May 15;103(10):1391-1398.

(2) HAART-induced increases in blood lymphocytes are of the CD4+ CD25+ 
phenotype (along with CD38 and CD44) (David Ho, 9th International 
Congress of Immunology, 1995), which are antigenic nonspecific 
suppressors (Thornton AM, Shevach EM. Suppressor effector function of 
CD4+CD25+ immunoregulatory T cells is antigen nonspecific. J Immunol 
2000 Jan 1;164(1):183-90). 

(3) Clerici M,* Seminari E, Suter F, Castelli F, Pan A, Biasin M, 
Colombo F, Trabattoni D, Maggiolo F, Carosi G, Maserti R (for the Master
Group). Different immunologic profiles characterize HIV infection in 
highly active antiretroviral therapy-treated and antiretroviral-naive 
patients with undetectable viraemia. AIDS 2000 Jan 28; 14:109-116.

(3) Soudeyns H, Campi G, Rizzardi GP, Lenge C, Demarest JF, Tambussi G, 
Lazzarin A, Kaufmann D, Casorati G, Corey L, Pantaleo G. Initiation of 
antiretroviral therapy during primary HIV-1 infection induces rapid 
stabilization of the T-cell receptor beta chain repertoire and reduces 
the level of T-cell oligoclonality. Blood 2000 Mar 1;95(5):1743-1751.

(3) Giorgi JV, Majchrowicz MA, Johnson TD, Hultin P, Matud J, Detels R. 
Immunologic effects of combined protease inhibitor and reverse 
transcriptase inhibitor therapy in previously treated chronic HIV-1 
infection. AIDS 1998 Oct 1;12:1833-1844

(3) Andre P, Groettrup M, Klenerman P, de Giuli R, Booth BL Jr, 
Cerundolo V, Bonneville M, Jotereau F, Zinkernagel RM, Lotteau V. An 
inhibitor of HIV-1 protease modulates proteasome activity, antigen 
presentation, and T cell responses. Proc Natl Acad Sci U S A 1998 Oct 
27;95(22):13120-13124 

(4) Al-Harthi L, Roebuck KA, Kessler H, Landay A. Inhibition of 
cytokine-driven human immunodeficiency virus type 1 replication by 
protease inhibitor. Journal of Infectious Diseases 176:1175-1179 (Nov 
1997).

(4) Andersson J, Fehniger TE, Patterson BK, Pottage J, Agnoli M, Jones 
P, Behbahani H, Landay L. Early reduction of immune activation in 
lymphoid tissue following highly active HIV therapy. AIDS 1998 
Jul 30;12:F123-F129.

(5) Markowitz M. Resistance, fitness, adherence, and potency: mapping 
the paths to virologic failure. JAMA 2000 Jan 12;283(2):250-1 

(5) Havlir DV, Hellmann NS, Petropoulos CJ, Whitcomb JM, Collier AC, 
Hirsch MS, Tebas P, Sommadossi JP, Richman DD. Drug susceptibility in 
HIV infection after viral rebound in patients receiving indinavir-
containing regimens. JAMA 2000 Jan 12;283(2):229-34 

======= 



From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  9 00:22:04 2000
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From: Simon Worrall <worrall@biosci.uq.edu.au>
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Subject: Re: I'm not a specialist...
Date: Thu, 09 Mar 2000 10:20:12 +1000
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You need a mol wt of ~1.5 kDa before something is immunogenic.  To raise
antibodies against smaller molecules they must be attached to a carrier
molecule, usually a protein.  They are then HAPTENS and immunogenic.
Antibodies can then be raised to the hapten and the carrier.

Glycolipids and nucleic acids are also immunogenic together with large
xenobiotic compounds.

Simon Worrall
Lecturer in Biochemistry
University of Queensland
Australia




From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  9 09:20:17 2000
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From: rubendaniel@my-deja.com
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Subject: fetal calf serum
Date: Thu, 09 Mar 2000 09:13:00 GMT
Organization: Deja.com - Before you buy.
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Hi everybody,
This is really a curiosity more than technical problem. What's the
reason for using fetal calf serum to make cell cultures??. Why not, for
example, newborn calf is usually cheaper?. All the companies I called
said that such serum came from animals less than 10-12 days old, so if
the animal is healthy what's the reason for not using that thing?


Sent via Deja.com http://www.deja.com/
Before you buy.


From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  9 14:36:44 2000
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From: Pierre =?iso-8859-1?Q?Commer=E7on?= <pcomm@univ-lyon1.fr>
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Subject: Ventana ????
Date: Thu, 09 Mar 2000 15:36:15 +0100
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Hello,

I'am very interested to buy an Ventana immunology automatized system.

Some people say that the results with it are not good (important
background...)

What is your experience with Ventana immunology automatized system ?

Have you some problems ?

Thanks a lot

Pierre

pcomm@univ-lyon1.fr



From owner-immuno@hgmp.mrc.ac.uk  Thu Mar  9 18:07:31 2000
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