Eczemax- There are several different types of eczema,many of which look
similar but have very different causes and treatments. The first step
in effective treatment of eczema is a correct diagnosis.We are
providing herbal treatment for the cure of eczema.All kinds of eczema
has been treated successfully.

http://www.herbaalex.com/eczemax.htm

Dermarine- A herbal treatment for severe kinds of leucoderma.Herbal
Medicine has very encouraging results in leucoderma. Acquired white
spots like due to burns or injuries are also treated successfully. The
duration and success of treatment depends on extend of the patches and
the duration of the illness. Big patches require more days whereas
small spots yield faster.

http://www.herbaalex.com/dermarine.htm

Mass Production and Purification

"…analysis of the proteins demands mass production and purification" —
Luc Montagnier 1997.

Purification of retroviruses is achieved by banding culture material in
sucrose density gradients.  A drop of culture supernatant is placed on top
of a column of sucrose solution of increasing density in a test tube.  The
tube is spun at high speeds for several hours and during this time the
retroviral particles, if present, travel though the gradient until they
encounter sucrose of the same density.  When they do, they stop and thus
concentrate.

In 1983 Professor Montagnier claimed to have discovered HIV based on this
method.  Material which banded at 1.16 gm/ml he and his colleagues called
pure virus.  One of the three proteins in this material, which reacted
with AIDS patient serum, was said to be a unique, HIV p24 protein. 
Although it was long considered mandatory to take an electron micrograph
to prove that gradient purified material contained retroviral particles
and nothing else but retrovirus particles, no such EM was ever published. 
This caveat, which is really no more than commonsense, to exclude that
there may not actually be a retrovirus, had in fact been listed as
requirement by two of Montagnier’s co-authors a decade earlier.  Despite
this omission, such banded material has been used by all HIV researchers
to obtain proteins, and RNA, to use a diagnostic agents to prove HIV
infection.

The first EMs of what was called purified HIV did not appear until
fourteen years afterwards.  This EM and the one following were published
in March 1997 in Virology.  This EM is from a Franco/German collaboration
which includes Hans Gelderblom from the Koch Institute in Berlin.  The
second is from the US National Cancer Institute.  In both slides the upper
two EMs are density gradient “purified HIV” and the lower EM a density
gradient of a non-infected culture.  Obviously, whatever these appearances
represent, nothing has been purified.  The authors admit this.  They also
claim that in the infected cultures, amongst all the contaminating
cellular material, there are a small number of particles which are a
retrovirus and are HIV.  But they don’t provide any proof.  In fact in
this slide there are two “HIV” particles in the non-infected material but
none of the particles in this or the NCI slide

have the appearance of retroviruses, let alone a specific retrovirus.  For
example, the “HIV” particles in this slide are two and half times the
diameter of any known retrovirus.  This is equivalent to a 15 foot man. 
To account for the appearances on these EMs the authors adopted the term
“co-purification”.  (You like your whisky neat but when the barman forgets
he leans over and tells you not to worry because the ginger ale
co-purifies).

"I repeat, we did not purify" Luc Montagnier, Pasteur Institute Interview
July 1997

Of significant interest, in a 1997 interview, Professor Montagnier said he
did not purify his 1983 HIV.  And that despite a Roman effort, he was
unable to find any particles with the morphology typical of retroviruses
in his gradient purified virus.  This interview was published by Huw
Christie in Continuum and a video tape copy is sitting on the table in
front of where I am sitting.  (This video was later given to the South
African Government after obtaining permission from its copyright owner).

If you perform a protein electrophoresis on the infected and non-infected
gradient purified material, you get this picture.  The only differences
between lane A , which is non-infected, and lanes B and C, which are, are
quantitative, not qualitative.  The bands labeled HIV down the bottom of
lanes B and C can also be seen, although not strongly, in the non-infected
specimen.  This could be explained by the different culture conditions. 
The infected cultures originate from AIDS patients who are highly oxidised
and these cultures are chemically stimulated.  And this material used to
“infect” these cultures already contains these proteins whereas the lane A
cultures are cultured on their own.  This same data was published in an
earlier paper by the same authors but without labels indicating viral
proteins.  We asked the senior author how they proved the strong bands
were HIV proteins.  His reply did not mention any such proof but merely
informed us that the labels were added at the suggestion of the editor to
better orientate the reader.   Independent data show that the proteins
labelled p24 and p18 have been found in a wide variety of uninfected human
tissues using AIDS sera and monoclonal antibodies to the so called “HIV”
proteins.  And where are the rest of the so called HIV proteins in this
“purified” virus?  Where are p41 and p65 and p120 and p160?  In other
words, these data are better explained by HIV proteins being not viral but
cellular.   In fact there are much other, independent data proving that
all the “HIV” proteins are cellular or, at the very least, non-specific.

In 1983 Montagnier declared that his p45 (now p41) protein is cellular
actin which “contaminated” his “purified” virus.  He reiterated this in
1996.  Others have proven that actin is a component of pure HIV.  HIV
researchers accept that the p160 protein is present only in cell cultures,
not HIV itself.  But p160 is one of the HIV antigens used in the Western
blot and is presumably also present in the HIV ELISA.  This means the
method used to obtain the HIV proteins for the WB does not use pure virus
as we can now readily accept given the EMs of “purified HIV”.  But there
is another explanation.

In 1989 Pinter and his colleagues did a chemical analysis of the so called
HIV glycoproteins present in the WB and found that p120 and p160 are
oligomers of p41.  They went so far as to warn that “Confusion over the
identification of these bands has resulted in incorrect conclusions…some
clinical specimens may been identified erroneously as seropositive…”

The non-specificity of the p24 antigen test is so obvious that it is
accepted by no less an authority on HIV testing than Philip Mortimer and
his colleagues from the UK Public Health Laboratory Service, "Experience
has shown that neither HIV culture nor tests for p24 antigen are of much
value in diagnostic testing. They may be insensitive and/or
non-specific".  p24 arises in cultures of non-infected individuals and in
fact the highest levels of the p24 HIV antigen are reported not from AIDS
patients but from no risk, non-HIV-infected organ transplant recipients.

The “HIV” Proteins

Henderson (1987) studied the p30-32 and p34-36 of "HIV purified by double
banding" in sucrose density gradients. Comparison with the amino-acid
sequences of these proteins with Class II histocompatability DR proteins
proved that "the DR alpha and beta chains appeared to be identical to the
p34-36 and p30-32 proteins respectively” Cellular origin also acknowledged
by other HIV experts such as Arthur (1995).

AIDS sera as well as monoclonal antibodies to the HIV p18 protein bind to
a wide variety of tissues from non-AIDS, non-risk, non antibody positive
patients and, if we look at the normal human placenta in a little more
detail,

Faulk and Labarrere (1991) studied immunocytochemical reactivity using
poly- and monoclonal antibodies. “Placentae from 25 normal term
pregnancies were collected by vaginal delivery…Antigens gp120 and p17
were identified in normal chorionic villi…Antigen p24…in villous
mesenchymal cells…localized to HLA-DR positive cells”

Thus, using antibody probes including monoclonals, three of the HIV
specific proteins show up in the placentas of non-HIV-infected women.

Thus, if gradient purified infected material consists of the same proteins
as uninfected material,  and does not contain retroviral particles, and is
not pure, then it is difficult to see how anyone can refer to this
material as purified HIV.  And use it for diagnostic purposed to pronounce
humans infected with a particular lethal retrovirus, HIV.

Well, regardless of the origin of these proteins, AIDS patients most
certainly have antibodies that react with these proteins and these
reactions correlate with either having AIDS or developing and dying of
AIDS.  Or being in a risk group.  Of this there can be no doubt.  The
problem for the Perth group, is how to explain this.  Well we can only
suggest an explanation.  Thanks to Kashala and Muller and others we know
that antibodies to mycobacteria and fungi such as Candida albicans bind to
the proteins present in the HIV antibody test kits.  And mycobacteria and
fungal diseases comprise about 90% of AIDS diagnoses.  Thus some, perhaps
quite a lot, of the reactivity might be explained on this basis.  AIDS
patients have a plethora of autoantibodies and this may explain further
reactivity.  And under the guise of the immune activation that accompanies
AIDS, we can not discount non-specific antibody production and other
cross-reactivities.  But the problem for us all, is whether these
reactions are caused by infection with an AIDS causing retrovirus.  And is
this all the time, some of the time or never?  Is there anything we do to
resolve this conundrum?  Yes there is.  We can walk humbly up to Mother
Nature and ask for her help.   She will tell you the only way to answer
this question is to use a gold standard.

Use the HIV gold standard. Compare the antibody reactions with the virus.
Until you do that you’re just staring at entrails.

Unfortunately, HIV isolation is problematic in the extreme.  When you
analyse the detail, at best HIV isolation consists of a series of
non-specific phenomena.  Measurement of reverse transcription, detection
of particles in culture fluids, antibody/antigen reactions all have
non-retroviral, non-infectious causes.  But we can appreciate that twenty
years ago, under such intense
…

Science, Vol 298, Issue 5599, 1727-1728 , 29 November 2002

HISTORICAL ESSAY:
A History of HIV Discovery
Luc Montagnier*

In 1972, Jacques Monod asked me to create a research unit in the new
virology department of the Pasteur Institute. I baptized it the viral
oncology unit because I shared the belief of many biologists that
certain human cancers could be caused by viruses, in particular by
retroviruses. I had some experience with chicken oncogenic viruses,
having confirmed with the late Philippe Vigier the existence of
infectious transforming DNA in chicken cells infected with Rous
Sarcoma virus (first described by Hill and Hillova) (1). Yet, despite
a well-funded effort, the "virus cancer program" failed to reveal a
retrovirus that could cause human cancer.

In 1977, as the viral oncology unit became interested in the action of
interferon, I had an illuminating idea: Perhaps we couldn’t isolate
retroviruses from human cancers because their expression was inhibited
by production of endogenous interferon. If we could neutralize this
effect by treating cancer cells with antiserum against interferon, we
might be able to detect a human oncogenic retrovirus. About this time,
Jean Claude Chermann and his young assistant Françoise Sinoussi, both
with expertise in mouse retroviruses, joined the unit. First, we
tested the idea in mouse cells and, indeed, production of exogeneous
and even endogeneous retroviruses could be boosted by treating cells
with low doses of antiserum to mouse interferon (2). Next, we
investigated human cancers, selecting acute and chronic lymphocytic
leukemias and breast cancers for study. We used the new T cell growth
factor (now called interleukin-2) discovered in Robert Gallo’s
laboratory to make short-term T lymphocyte cultures from cancer
patients. We hoped that the retrovirus might be hiding not only in
human cancer cells but also in T cell subsets. We examined many
lymphocyte samples from cancer patients, each time culturing the cells
with and without antiserum to human interferon. Françoise Sinoussi
measured reverse transcriptase (RT) activity (a retroviral enzyme) in
the culture supernatants. We had a few (false) positive results due to
RT activity associated with mycoplasma contamination of our T cell
cultures. In 1982, using a DNA probe from the mouse mammary tumor
virus, Michel Crepin detected by molecular hybridization a DNA
sequence in a human breast tumor that resembled a sequence in the
mouse oncogenic retrovirus (3). Strikingly, the same DNA sequence
could be recovered from cultured T lymphocytes taken from the cancer
patient.

It was at this time that I first heard about the "gay disease." There
were only a few patients with this disease in France, but Gallo’s idea
that a retrovirus was the cause had already crossed the Atlantic. His
idea was disseminated by a small group of clinicians and immunologists
led by Jacques Leibowitch and Willy Rozenbaum. At the end of 1982,
Françoise Brun-Vezinet, a former student of mine and a member of this
group, proposed that we collaborate to discover if a retrovirus was
the cause of this disease, now called AIDS.

We were ready to start because my laboratory was equipped to hunt for
lymphotropic retroviruses in human T cell cultures. In addition, there
was a risk that human plasma collected from blood in the United States
and used by the Pasteur Institute’s industrial subsidiary to prepare a
hepatitis B vaccine might be contaminated by the AIDS agent. On 3
January 1983, Françoise Brun-Vezinet obtained a lymph node biopsy from
one of Rozenbaum’s patients, a young gay man (BRU) with a
lymphadenopathy in the neck. I minced the lymph node, dissociated the
fragments into single cells, and cultured the T lymphocytes with
interleukin-2 and antiserum to human interferon. Fifteen days later,
Françoise Sinoussi (by then Barré-Sinoussi) found the first traces of
RT in the supernatant of the lymphocyte culture, indicating the
presence of a retrovirus. The only retroviruses then known were the
human T cell leukemia viruses, HTLV-1 and HTLV-2, identified by
Gallo’s group. So, we tested whether the viral proteins in the
supernatant could be recognized by Gallo’s antibodies against HTLV.
Surprisingly, our labeled viral supernatant could not be immune
precipitated with the HTLV antibodies, but could be precipitated with
the patient’s own serum (4). A protein with a molecular mass of about
25 kD precipitated by the patient’s serum seemed to be the counterpart
of the p24 protein of HTLV-1. The virus could not be isolated from
blood lymphocytes, a fact that is now explained by the early stage
(lymphadenopathy) of this patient’s disease when the virus is almost
exclusively located in lymphatic tissues. Louis Pasteur’s quote that
"luck in science smiles on prepared minds" certainly applied to us. We
received a biopsy from another young gay male patient (MOI), who was
infected with both HTLV and the new lymphadenopathy-associated virus.
If MOI had been our first patient, we would have been very confused.

A few months later, I received a blood sample from a young hemophiliac
(LOI) with full-blown AIDS, and blood and lymph node samples from a
young gay man (LAI) with advanced Kaposi’s sarcoma. The LAI virus
could be isolated from the patient’s blood cells and grew very quickly
in the patient’s cultured T lymphocytes, killing them as well as
killing T lymphocytes from blood donors. In September, we isolated a
similar virus from the blood of a Zairian woman, ELI, who died of AIDS
a week later. All of the isolated viruses showed cross-reactivity
between their gag proteins (p25 and p18) (5). The viruses isolated
from full-blown AIDS patients were more aggressive than the BRU virus,
and so I called them immune deficiency-associated viruses (IDAV). The
viruses like BRU that were isolated from patients who only suffered
from lymphadenopathy were termed lymphadenopathy-associated viruses,
or LAV. This classification corresponded to the later terminology of
syncitium and nonsyncitium-inducing strains.

The retrovirus was new, as was the disease. My collaborator, the
electron microscopist Charles Dauguet, showed me pictures of the viral
particles whose dark, cone-shaped centers suggested that this virus
was not the same as HTLV. Fellow virologist Edwald Edlinger suggested
that I compare the new virus with animal lentiviruses, and, indeed,
the pictures of viral particles we obtained in June 1983 looked
identical! As I told Robert Gallo, I was convinced that we were
dealing with a virus quite different from the HTLV family.

To better characterize the new virus, we tried (unsuccessfully) to
grow the BRU isolate in different T cell lines. If we had tried the
LAI isolate instead, we would have been able to grow the virus without
any trouble. In October 1983, we were finally able to grow the BRU
isolate in Epstein-Barr virus-transformed B cell lines, although we
discovered later that the LAI virus had contaminated our BRU culture
(6). At least six laboratories received the LAI sample (under the name
BRU) from our group and experienced the same contamination. We think
that the LAI virus readily contaminated the BRU culture because it
associates with a mycoplasma species, Mycoplasma pirum, usually
present in T cell lines. This physical association makes a fraction of
the LAI virus highly infectious, and, in fact, this fraction can be
neutralized with antibodies against M. pirum. As mycoplasmas are
common contaminants of cultured cells, an infectious pseudotype virus
(LAI associated with M. pirum) may have caused several contaminations
between 1983 and 1984 in different laboratories.

New evidence that this strange retrovirus was the cause of AIDS came
from our team in the fall of 1983 and the winter of 1984 (7). We
observed a high frequency of antibodies against the virus in
lymphadenopathy patients, and noted the favored tropism of this virus
for CD4+ T lymphocytes. Our results were still controversial, however,
and we had difficulty in obtaining the funding needed to better
characterize the virus and to develop a blood test. The tide only
turned in France when Robert Gallo and his group in the United States
made a similar discovery. In the spring of 1984, Gallo published more
convincing evidence that HIV causes AIDS (8) (see the Viewpoint by
Gallo on page 1728), a finding that was confirmed by Jay Levy’s group
(9). In 1985 came the cloning and sequencing of the HIV genome with
identification of new open reading frames specific for lentiviruses
(10). This was followed by identification of the HIV large surface
glycoprotein (11) and of T cell CD4 as the receptor for HIV (12, 13).
In 1986, HIV-2 was isolated from West African patients (14).

Over the past 20 years, the scientific and legal controversies between
our team and Gallo’s group have faded. We are left with the salient
fact that HIV was identified and shown to be the cause of AIDS less
than 2 1/2 years after this disease was first identified. It took only
another 2 years for blood tests to become commercially available,
reducing almost to zero the transmission of AIDS through blood
transfusion in developed countries. In 1987, the first anti-HIV drug,
AZT, which blocks HIV RT activity, was introduced. With the arrival of
the HIV protease inhibitors and triple drug therapy in 1995, many
patients are alive today who would otherwise have died.

But we must not be complacent–the task ahead is immense. We still do
not understand the origin of the AIDS epidemic; the slow destruction
of the immune system by factors in addition to HIV infection of CD4+ T
cells; the importance of cofactors in AIDS progression and virus
transmission; and the nature of the HIV reservoir that resists triple
drug therapy. The next wave of advances in the fight against this
worldwide scourge will require the contribution and energy of us all.

References and Notes

   1. P. Vigier, L. Montagnier Int. J. Cancer 15, 67 (1975). [Medline]
   2. F.
…

How does the Red Cross test blood?

——————————————————————————–

COMMUNITY BRIEFING: Multi-drug Resistant, Fast Progressing HIV in NYC
Project Inform Press Statement on the New York City Department of
Health Report of a "Super" Strain of HIV
Commentary: How Important is the New York Resistance Case?
U.S. NIH Chief Seeks Conflict-of-Interest Summit
Higher HIV Load Worsens Neuropsychological Functioning in Children
Transient Blips in HIV Viremia Not Clinically Significant
HIV Infection Increases Risk of Other STDs in Women
HIV Co-receptor Use in the Blood and Central Nervous System Differs in
20% of Patients
Low Weight in Women a Risk Factor for Severe Nevirapine Liver
Toxicities
Methamphetamine Use Can Worsen Brain Damage Caused by HIV Infection
HIV ‘Could Destroy Cancer Cells’
Shape of Unbound HIV Gp120 Elucidated
GBV-C Infection Does Not Protect Against CD4+ Cell Loss or HIV
Progression
Risk of MI Increases with Longer HAART Exposure
Imatinib Can Produce Rapid Regression of AIDS-related KS Lesions
HIV Tat Protein Implicated in Amyloid Beta Accumulation in the Brain
Differences in HIV Viral Load Between Men and Women Can’t be Explained
by CD8 Response, Finds Study
Fish Oils Can Reverse High Blood Lipids Caused by Antiretrovirals
Long-term CD4 Increase on HAART Averages 250-350 Cells, Plateaus After
3-4 Years
Addition of Capravirine to a Three-drug Regimen Not Beneficial in
Patients with NNRTI Resistance
Therapeutic Drug Monitoring Useful for Improving Treatment Outcomes in
Many Patients Taking HAART
MRSA in HIV-positive Patients Often Community Acquired, Associated
with HIV Disease Severity
Two New Drug Classes Given to People with HIV for the First Time
Therapeutic Vaccine Plus Interleukin-2 Shows Best Viral Control in
Treatment Breaks
ADVOCACY ALERT: Call Your U.S. Senators Before March 7—Or We May Lose

Also: "This Week @ The CFA"

Note: As many of you are already aware, The Rita! Weekly Newsletter
was not delivered last week. The editor apologizes for any
inconvenience this may have caused. This edition of the newsletter
contains news from Monday, February 14, 2005 though Friday, February
25, 2005. Thank you.

——————————————————————————–

1. COMMUNITY BRIEFING: Multi-drug Resistant, Fast Progressing HIV in
NYC
Community HIV/AIDS Champ Mobilization Project (2/25/05)

In the past several weeks, there has been much media attention on a
case of a man with HIV who progressed to an AIDS diagnosis in a
relatively short time, and whose virus is resistant to many kinds of
AIDS drugs. This has raised alarm for many people in a time in which
there is much fear of drug resistance as well as concerns about the
challenges of HIV prevention. This fact sheet has been created by HIV
prevention and treatment activists to supplement available materials
on this case. It will be updated as more information becomes
available, and was completed on February 24, 2004. We hope it will
present background information on this case and provoke additional
inquiry to understand more about its implications. In addition, it
presents historical data that might be useful in putting this case
into context. It does not repeat basic information on HIV prevention,
crystal meth, or the importance of medication adherence, as these are
available elsewhere. In addition, it does not address significant
concerns about the way this story was released and its subsequent
coverage in the media, which are initiated in other document and still
require additional discussion. We have collected some of these
additional materials on a webpage, including a community sign-on
letter, organizational statements, and a service provider advisory
from the New York State Department of Health [please see below].

For more information, contact:
Richard Jefferys, TAG / Richard.jeffe…@verizon.net o 212-253-7922
Julie Davids, CHAMP / jdav…@champnetwork.org o 212-966-0466 x 1206

[To access the fact sheet and other information please visit:
http://www.champnetwork.org/index.php?name=newcase ]

2. Project Inform Press Statement on the New York City Department of
Health Report of a "Super" Strain of HIV
Project Inform (2/11/2005)

The New York City Department of Health and Mental Hygiene, in
collaboration with the Aaron Diamond AIDS Research Center, released a
press statement today reporting on a finding of man newly infected
with a multi-drug resistant strain of HIV. The report described the
man as being resistant to three classes of anti-HIV drugs and as
having a particularly virulent strain of HIV. Although the
transmission of drug-resistant HIV is a serious concern, Project
Inform believes that the current reports may be unnecessarily alarming
to the public. There is currently too little information available,
and doctors have followed the patient for too short a time, to draw
any conclusions about the significance of this situation. However,
several aspects of the story being reported warrant further
explanation.

First, there is nothing new about people becoming infected with
resistant strains of HIV, including multi-drug resistant strains. Such
cases have been reported at scientific conferences for the last
several years. In a study reported in the Journal AIDS : Volume 18(10)
2 July 2004, author Douglas Richman reports that "… Resistance to all
three drug classes was detected in an estimated 13.1% (of 17,300
patients) …" If triple class drug resistance is as common in the U.S.
as Dr. Richman reports, it is likely that we will continue to see some
portion of newly infected patients present with this level of
resistance.

The advisory and press statement from New York City suggests that the
patient is virtually untreatable, but this statement seems
contradicted by other claims in the same report. The article says that
the patient is responsive to the drug Fuzeon and may be responsive to
Sustiva. If responsive to Sustiva, he is not "resistant to 3 classes
of HIV medication" as claimed in the headline.

Another aspect of the reported case which is troubling is that the
patient has a low CD4+ count. This was being interpreted as a sign of
very rapid disease progression. However, it is common for people newly
infected with HIV to have a period of low CD4+ counts and high viral
load often lasting as long as 6 months after initial infection. Since
the researchers involved suspect that the patient was infected in
December 2004, it is not possible to determine at this time whether
the patient’s low CD4+ count suggests a particularly aggressive form
of HIV or whether it is simply a reflection of the short time since
infection. Only longer follow-up will answer this question.

Another concern stated by the researchers is that the patient has what
is known as a "dual tropic" form of HIV. This means that the virus can
use either of two different secondary receptors on cells. This
characteristic is usually associated with virus seen in people with
advanced disease. At the very least, this means the patient acquired
the virus from someone with an advanced form of the disease. There is
as yet no evidence though that this means he will retain this form of
the virus over time.

We believe that it is premature to conclude that this event represents
evidence of a "superbug" or a particularly virulent strain of HIV, or
that the patient is "untreatable" or will suffer a particularly rapid
disease progression. These conclusions can neither be ruled in nor
ruled out at this time. What’s needed is an extensive period of
follow-up and careful continued monitoring of the patient. In many
previously reported cases of people presenting with multi-drug
resistance, the characteristics of their virus changed over time and
they were able to develop normal sensitivity to the available drugs.

HIV infection presents a complex mix of factors that determine the
outcome in individual patients. These include the characteristics of
the initial virus a person acquires, but also how a person’s immune
system responds to the virus, and in turn, how the virus evolves in
reaction to the immune system and any drugs used to treat it. No
single snapshot of data can accurately predict the course of disease
for an individual.

Project Inform shares the concern of scientists and public health
workers over the spread of resistant virus, but we also recognize how
difficult it is to predict the significance of any individual case and
what it may or may not mean for the at-risk populations. Every effort
must be made to stop the spread of HIV, regardless of whether it is in
drug resistant or drug sensitive form. We also believe that new
information should be studied carefully and interpreted with caution
and that care should be taken not to cause undue alarm when the facts
are uncertain, as they are in this case.

Our understanding of the current situation is based on extended
conversations with a number of AIDS experts and researchers, who like
us, can only base their assessments on the limited information
currently available. We strongly support the efforts of the New York
City Department of Health and Mental Hygiene to continue following
this case and to determine how frequently similar types of HIV
transmission might be occurring.

Established in 1985 as a national non-profit community-based
organization, Project Inform is the nation’s leading independent
HIV/AIDS treatment information and advocacy resource. Relied upon for
information about optimal treatment strategies, access to care and
treatment, and advances in research, Project Inform is committed to an
integrated approach to treatment education, advocacy and inspiration
for people living with HIV/AIDS, their family, friends, caregivers,
healthcare and service providers.

Treatment Hotline: 800-822-7422 (toll-free) or 415-558-9051 (in the
San Francisco Bay Area and internationally)
Hotline hours: Monday, Wednesday–Friday, 9am–4pm and
…

Hello,

I have been rolling around the idea of starting a Wiki to promote positive
changes in the multiple facets of Aids (research, alternative therapies,
activism, rights, et cetera). I registered AidsWiki.org back in August, but
became preoccupied with other interests (finding a salaried position, for
one thing LOL). Now that I’m happily reemployed I’m again pondering how best
to spend some time on this project. Would any members of this newsgroup have
thoughts, warnings, ideas, or links to resources?

Best regards,

Jeff

Hidden Facts and Dangers of HIV Tests
What’s in the Fine Print

Remarkable information about HIV tests including the fact that no HIV
test
has ever been approved by the US Food and Drug Administration for the
actual diagnosing of HIV infection.

Few doctors, clinics, journalists, or AIDS organizations know that all
current HIV tests are approved only as screening tests, prognostic tests
(for predicting a possible future outcome) or as "an aid in diagnosis"
and
are not intended to be used for determining if a person actually has HIV.

The FDA’s lack of such approval speaks to the fact that no HIV test can
directly detect or quantify HIV or determine the presence of specific HIV
antibodies in human blood.
Recent changes in the fine print of the test kits acknowledge this little
known data and seem to indicate a change of thought with regard to the
role of HIV in AIDS.

From 1984 until last year, test literature contained the very certain
statement that "AIDS is CAUSED by HIV." Then in November of 2002, a new
test kit started what now seems to be a trend toward rethinking the
causal
link between HIV and AIDS. It states, "AIDS, AIDS related complex and
pre-AIDS are THOUGHT TO BE CAUSED by HIV." (OraQuick Rapid HIV-1 Antibody
Test, OraSure Technologies, Inc)

Now it appears we’ve gone from "HIV is thought to cause AIDS," to
something even more uncertain: "Published data indicate A STRONG
CORRELATION between the acquired immunodeficiency syndrome (AIDS) and a
retrovirus REFERRED TO as Human Immunodeficiency Virus (HIV)."

This last quote is found in the package insert for a new ELISA test
(Vironostika HIV-1 Plus O Microelisa System) the FDA approved in June
2003.

The entire package insert can be downloaded from
http://www.fda.gov/cber/pma/P020066.htm

According to Alive & Well advisor Dr Rodney Richards, a chemist and
co-creator of the very first HIV test, as of June 2003, the number of FDA
approved tests that contain the term HIV or LAV (the old school term for
the so-called virus) have risen to 36. Of these, 13 have been approved in
just the last three years.

Richards points out that "despite the increased number of HIV tests,
there
is still no manufacturer that claims their test can be used to diagnose
infection with HIV. All of the RNA based tests for viral load and
genotyping clearly state they are ‘NOT intended for use in diagnosing HIV
infection.’

Instead of an indication for use in detecting or quantifying the actual
virus, these tests are approved only for prognosis or monitoring therapy
for people who doctors assume are infected.?

Richards is working on a document to clarify what HIV test manufacturers
mean by the terms "prognosis," "monitoring of therapy," and "aid in the
diagnosis of HIV." His report will focus on what the tests cannot do
(diagnose HIV infection) and what exactly they can.
At first glance, the rapid tests may appear relatively benign since the
manufacturers clearly emphasize that "preliminary positives" must be
confirmed with follow up testing.

This emphasis is due to the fact that the accuracy of the rapid tests? is
widely known to be more questionable than the already dubious HIV ELISA
or
Western Blot. But the notion that medical personnel will await
confirmation of results before insisting patients take action is entirely
misguided since the true market for rapid tests is pregnant women in
labor

Incredibly, the recommendation to misuse rapid tests for women in labor
comes directly from the Deputy Commissioner of the FDA himself, Dr.
Lester
M Crawford.

The good doctor says "OraQuick will be a great help in identifying
pregnant HIV-infected women going into labor who were not tested during
pregnancy so that precautionary steps can be taken to block their
newborns
from being infected with HIV." (FDA News, November 7, 2002)

These precautionary steps include IV infusion of the toxic chemotherapy
AZT during labor, C-section delivery, six weeks of mandatory AZT
treatment
for the baby regardless of their own HIV status, and orders to the mother
not to breastfeed.

Even though chemotherapy, surgery and denial of normal feeding are based
on preliminary results from a test never approved for detecting HIV
infection, a mother who declines such intervention risks losing custody
of
her child.

Perhaps more remarkable than official calls for misuse of rapid tests is
a
disclosure by the manufacturer of the OraQuick that 7% of women with a
history of prior pregnancy will score falsely positive on their test.
Further, the manufacturer of the newly approved Reveal test didn’t even
evaluate their product in multiparous women.

Worse still, as Dr Richards points out, the rapid tests may soon be
routinely administered to women tested negative before labor. "Based on
the erroneous belief these tests can actually diagnose HIV infection,
doctors may want to retest women in labor who?ve previously come up
negative just to be sure they haven’t seroconverted in the mean time."

Another lucrative market for the rapid tests is among healthcare workers
who experience accidental needle sticks or other unintentional contact
with patient fluids. As Richard points out, this opens a Pandora?s box of
potential life-altering situations.

"Imagine a nurse sticks herself with a used needle. Ora-Sure gives her
the
impression she can find out quickly if that needle is contaminated with
HIV. Should the needle score positive, she would then be urged to start
prophylactic chemotherapy right away.
Of course, if the needle scores positive, hospitals would most likely
feel
an ethical responsibility to
inform the patient and to urge them to also start ‘saving their lives’
with AIDS meds. Since there are 600,000 to 1,000,000 accidental needles
sticks in the US annually, this is a huge market for both the test and
treatment manufacturers."

The great influence of drug and test manufacturers on public health
policy, media presentations and among AIDS activist groups may mean that
the hidden dangers of rapid tests will remain unknown.

************
*AIDS MYTH*
************

Zimbabwe Resisting Facts in AIDS Epidemic
By JANE PERLEZSpecial to The New York Times. New York
Times (1857-Current file). New York, N.Y.:
Nov 24, 1989. pg. A7, 1 pgs

Document types:   article
Dateline:   BULAWAYO, Zimbabwe, Nov. 17
Section:   INTERNATIONAL
ISSN/ISBN:   03624331
Text Word Count   664
Document URL:

Abstract (Document Summary)
BULAWAYO, Zimbabwe, Nov. 17 — Ronnie Mutimusekwa, a
34-year-old street vendor who is infected with the AIDS virus, is
trying to help educate the public about the disease in Zimbabwe,
where people are said to doubt its rapid spread.

************
*AIDS FACT*
************

Zimbabwe population:

*************

This quote was posted at MSN group Dissident-Action and what a
wonderful observation.

From: dr_taciturn

"If ever there was in the world a warrented and proven history, it is
that of vampires. Nothing is lacking; official reports, testimonials of
persons of standing, of surgeons, of clergymen, of judges; the evidence
is all embracing." – Jean Jacques Rousseau.

They obviously know what they are talking about…