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medicine forum Guru

Joined: 02 May 2005
Posts: 1814

PostPosted: Fri Jul 14, 2006 9:20 pm    Post subject: AIDS Reply with quote


Science by press conference
Gallo's original Science papers, a relevant section of which is
reproduced here, claimed "isolation" of HIV only in 30.2% of adult AIDS
cases with Kaposi's sarcoma, and 47.6% of adult AIDS cases with
opportunistic infection. This is the evidence based on which Gallo,
with the blessings of Reagan's Secretary of Health and Human Services,
Margaret Heckler, told the world press on April 23th, 1984 (two weeks
before publication of the Science papers), that he had found the
"probable cause of AIDS"!

The word "probable" was forgotten within days, "HIV positivity", as
measured by Gallo's own test, was incorporated into the AIDS definition
and research into all other possible causes of AIDS ceased. Everyone
was happy- gay activists had their politically correct equal
opportunity killer that would surely strike heterosexuals any time now,
scientists like Gallo had billions of research funding coming their way
and people with AIDS or at risk for AIDS had new hope that this new
nightmare would soon be over. No one cared that Gallo had made an end
run around the scientific method. Results were already accepted as true
when they had not been discussed, critiqued or independently
replicated. No such process was possible anymore in the "foregone
conclusion" atmosphere created by Gallo's succesful PR stunt and the
official imprimatur given to his alleged discovery by the US

It was later revealed that Gallo had stolen his samples from French
researcher Luc Montagnier. A nasty fight about patent rights ensued
between the US and French government, during which the central question
of whether Gallo's results had any validity in the first place was
ignored. Eventually, the two governments settled on a compromise,
officially making Montagnier and Gallo "co-discoverers" of HIV. Gallo
was later convicted of science fraud for his research in "HIV
isolation" by a congressional investigation, the Dingell Inquiry.
Unfortunately, the United States government was not willing to risk a
debate on whether it had bet on the wrong horse and wasted almost a
decade and billions of research dollars on a phantom. The report was
soon forgotten and business continued as usual.

More details on Gallo's scientific misconduct can be found in Science
Fictions - A Scientific Mystery, a Massive Cover-Up and the Dark Legacy
of Robert Gallo by John Crewdson.


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medicine forum Guru Wannabe

Joined: 07 May 2005
Posts: 193

PostPosted: Fri Jul 14, 2006 10:19 pm    Post subject: Re: AIDS Reply with quote

Proof Derived from Koch's Postulates

Tim Teeter

The recent surge of publicity denying HIV's causal role in AIDS begs
an examination of the relationship between a specific microorganism
and a specific disease. The question is this: What scientific proof is
required to establish cause and effect?

HIV and AIDS-Related Diseases

AIDS is defined by the Centers for Disease Control and Prevention
(CDC) as the presence of a positive HIV antibody test and one or more
of the illnesses known as opportunistic infections (OIs) or a CD4 cell
count below 200 cells/mm3. AIDS wasting syndrome, which technically is
not considered an OI, and three cancers--non-Hodgkin's lymphoma,
Kaposi's sarcoma (KS), and cervical carcinoma--are AIDS-defining in
the presence of a positive HIV antibody test. HIV and AIDS have been
continuously linked in time, place, and certain population groups
(e.g., children born to HIV-infected mothers) since 1984, the year HIV
was discovered. Besides millions of cases of AIDS, some people
receiving cancer chemotherapy develop AIDS-like illnesses. And in
people receiving organ transplants, the immune system is deliberately
suppressed and AIDS-like illnesses can result. Neither of these two
examples, however, results in an AIDS diagnosis. Moreover, those
illnesses resolve when the causative medications are stopped.

Recent improvements in laboratory testing, particularly polymerase
chain reaction (PCR) testing, allow detection of HIV genetic material
in people with AIDS or a positive HIV antibody test result.
Interestingly, a 1995 study of 230,000 people with AIDS found that 168
were HIV-seronegative. Today it is known that the immune system
depletion characteristic of advanced HIV disease can suppress the
production of antibodies to HIV, which may explain this earlier

The vast majority of people with AIDS in resource-poor countries have
not had an HIV antibody test; even in developed countries, not all
people with AIDS have had viral load tests. Those who have had viral
load tests showing nondetectable virus generally have no additional
tests to confirm the presence of HIV genetic material.

However, the above facts, while strongly suggesting a relationship
between HIV and AIDS, do not by themselves establish a causal

Koch's Postulates

The German scientist Robert Koch (1843-1910) established four
requirements, or postulates, that must be demonstrated to prove that a
specific microorganism causes a particular disease:

1. The microorganism must be found in all cases of the disease.

2. It must be possible to isolate the microorganism from the host
and grow it in pure culture (in the laboratory).

3. The microorganism must reproduce the original disease when
introduced into an experimental animal.

4. The microorganism must be recoverable from that animal.

The scientific research community widely accepts that fulfillment of
these postulates demonstrates causality. Even scientists such as Peter
Duesberg, PhD, who says he believes that HIV does not cause AIDS,
accept that the postulates put forth by Robert Koch are sufficient to
establish causality. While in 1987 Dr. Duesberg noted that HIV did not
fit all of Koch's criteria, developments in HIV/AIDS research in the
13 years since that statement have shown that HIV does indeed fulfill
Koch's postulates as the cause of AIDS.

Conclusive Data from Reputable Scientific Research

Regarding postulate one, PCR testing allows researchers to document
cell-associated proviral HIV in persons with AIDS who have been tested
(proviral DNA detection is a research test, not one of the common
FDA-approved viral load tests). Prior to this technology, HIV was
often difficult to find. In addition, combining PCR testing with the
common viral load tests has documented the presence of HIV genes as
RNA freely floating in the blood plasma, outside of cells, in persons
with a positive antibody test not taking anti-HIV medication. (Viral
load testing looks for virus; the ELISA and Western blot tests look
for antibodies to HIV.)

Regarding postulate two, improvements in laboratory culture techniques
have allowed the growth of HIV in vitro (in laboratory models) from
blood samples obtained from persons with AIDS who have undergone such
testing and from almost all persons with a positive antibody test
without AIDS who have undergone such testing.

The last two postulates stipulate that inoculating the organism into
an animal model (i.e., exposing or infecting the animal) leads to the
same disease and that the organism is recoverable from that animal.
The evidence satisfying these postulates was established in 1997, when
Francis J. Novembre, PhD, and colleagues from Emory University in
Atlanta, GA, published in the Journal of Virology that a chimpanzee
inoculated with HIV ten years earlier had developed an AIDS-defining
OI. Prior to the OI, the HIV RNA viral load had increased (partially
documenting recovery of the organism from the animal model) and the
CD4 cell count had decreased in the chimpanzee. Cultures of blood from
the animal also were positive for HIV, establishing recoverability of
the organism. Subsequently, blood from that chimp was transfused into
a second, healthy chimpanzee. This second chimpanzee later had an
increase in the HIV viral load and a decrease in the CD4 cell count.

Prior to this 1997 report, fulfillment of Koch's third and fourth
postulates was lacking. Interestingly, the incubation period for
clinical AIDS in this chimpanzee, with whom humans share 98% gene
homology (structural similarity), was essentially equivalent to the
average incubation period in humans--ten years. This finding and
publication were reported in the September 1997 issue of BETA. While
evidence from one chimpanzee may not seem compelling to the lay
person, in the scientific arena and in conjunction with other,
cumulative data, it is considered persuasive. A good source of
information on this topic is www.niaid.nih.gov.

Ancillary and Epidemiologic Supporting Evidence

Several reports document the transmission of the organism to a human
host that reproduces the original disease, and the subsequent recovery
of the microorganism in that second person. For example, at least
three laboratory workers developed AIDS after accidental exposure to
concentrated HIV in the laboratory. All three developed
immunosuppression and related opportunistic diseases, including
Pneumocystis carinii pneumonia (PCP), following infection. In all
three cases, HIV was isolated, sequenced, and shown to be the
infecting strain of the virus.

In addition, the development of AIDS following known HIV
seroconversion has been repeatedly observed in widely diverse
populations, including each of the following:

* pediatric and adult blood transfusion cases

* hemophiliacs who received infected blood clotting factor protein

* monogamous sexual partners of those transfusion recipients

* health-care workers with accidental needlestick or other
occupational exposure, similar to the lab technicians described above

* mother-to-child transmission

* male-to-male and male-to-female sexual transmission

* injection drug users with secondary sexual transmission

* extremely rare outbreaks including transmission to dental
patients from an infected dentist (e.g., the Kimberly Bergalis case in

In conclusion, although the specific molecular mechanisms of HIV's
causative role in AIDS are not yet completely understood, Koch's
postulates have been fulfilled, thus establishing causality.

Tim Teeter is Associate Director of Treatment Support and Publications
at the San Francisco AIDS Foundation.

Related BETA Articles: "Special Report on HIV & AIDS"; "HIV is the
Only Cause of AIDS: The Potential for Journalism to Impact the Public

Selected Sources

Burnett, M. and White, D.O. Natural History of Infectious Disease.
Cambridge University Press, Cambridge. 1972.

Cohen, J. Fulfilling Koch's postulates. Science 2666(5191): 1647.
December 1994.

National Institute of Allergy and Infectious Diseases (NIAID) Fact
Sheet. The evidence that HIV causes AIDS. July 1995.

Novembre, F.J. and others. Development of AIDS in a chimpanzee
infected with human immunodeficiency virus type 1. Journal of Virology
71(5): 4086-4102. May 1997.

Weiss, R.A. and Jaffee, H.W. Duesberg, HIV, and AIDS. Nature
345(6277): 659. June 1990.

Page last updated 2 June 2000
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medicine forum Guru Wannabe

Joined: 07 May 2005
Posts: 193

PostPosted: Fri Jul 14, 2006 10:22 pm    Post subject: Re: AIDS Reply with quote

How HIV Causes AIDS
A significant component of the research effort of the National
Institute of Allergy and Infectious Diseases (NIAID) is devoted to the
pathogenesis of HIV (human immunodeficiency virus) disease. Studies on
pathogenesis address the complex mechanisms that result in the
destruction of the immune system of an HIV-infected person. A detailed
understanding of HIV and how it establishes infection and causes AIDS
(acquired immunodeficiency syndrome) is crucial to identifying and
developing effective drugs and vaccines to fight HIV and AIDS. This
fact sheet summarizes the state of knowledge in this area.

(Scientific terms printed in bold-faced type are defined in the
Glossary at the end of this document.)


Untreated HIV disease is characterized by a gradual deterioration of
immune function. Most notably, crucial immune cells called CD4
positive (CD4+) T cells are disabled and killed during the typical
course of infection. These cells, sometimes called “T-helper cells,”
play a central role in the immune response, signaling other cells in
the immune system to perform their special functions.

A healthy, uninfected person usually has 800 to 1,200 CD4+ T cells per
cubic millimeter (mm3) of blood. During untreated HIV infection, the
number of these cells in a person’s blood progressively declines. When
the CD4+ T cell count falls below 200/mm3, a person becomes
particularly vulnerable to the opportunistic infections and cancers
that typify AIDS, the end stage of HIV disease. People with AIDS often
suffer infections of the lungs, intestinal tract, brain, eyes, and
other organs, as well as debilitating weight loss, diarrhea,
neurologic conditions, and cancers such as Kaposi’s sarcoma and
certain types of lymphomas.

Most scientists think that HIV causes AIDS by directly inducing the
death of CD4+ T cells or interfering with their normal function, and
by triggering other events that weaken a person’s immune function. For
example, the network of signaling molecules that normally regulates a
person’s immune response is disrupted during HIV disease, impairing a
person’s ability to fight other infections. The HIV-mediated
destruction of the lymph nodes and related immunologic organs also
plays a major role in causing the immunosuppression seen in people
with AIDS. Immunosuppression by HIV is confirmed by the fact that
medicines, which interfere with the HIV lifecycle, preserve CD4+ T
cells and immune function as well as delay clinical illness.


Although HIV was first identified in 1983, studies of previously
stored blood samples indicate that the virus entered the U.S.
population sometime in the late 1970s. In the United States, 886,575
cases of AIDS, and 501,669 deaths among people with AIDS had been
reported to the Centers for Disease Control and Prevention (CDC) by
the end of 2002. Approximately 40,000 new HIV infections occur each
year in the United States, 70 percent of them among men and 30 percent
among women. Of the new infections, approximately 40 percent are from
male-to-male contact, 30 percent from heterosexual contact, and 25
percent from injection drug use. Minority groups in the United States
have also been disproportionately affected by the epidemic.

Worldwide, an estimated 38 million people were living with HIV/AIDS as
of December 2003, according to the Joint United Nations Programme on
HIV/AIDS (UNAIDS) . Through 2003, cumulative AIDS-associated deaths
worldwide numbered more than 20 million. Globally, approximately 5
million new HIV infections and approximately 3 million AIDS-related
deaths, including an estimated 490,000 children under 15 years old,
occurred in the year 2003 alone.


HIV belongs to a class of viruses called retroviruses . Retroviruses
are RNA (ribonucleic acid) viruses, and in order to replicate
(duplicate). they must make a DNA (deoxyribonucleic acid) copy of
their RNA. It is the DNA genes that allow the virus to replicate.

Like all viruses, HIV can replicate only inside cells, commandeering
the cell’s machinery to reproduce. Only HIV and other retroviruses,
however, once inside a cell, use an enzyme called reverse
transcriptase to convert their RNA into DNA, which can be incorporated
into the host cell’s genes.

Slow viruses

HIV belongs to a subgroup of retroviruses known as lentiviruses , or
“slow” viruses. The course of infection with these viruses is
characterized by a long interval between initial infection and the
onset of serious symptoms.

Other lentiviruses infect nonhuman species. For example, the feline
immunodeficiency virus (FIV) infects cats and the simian
immunodeficiency virus (SIV) infects monkeys and other nonhuman
primates. Like HIV in humans, these animal viruses primarily infect
immune system cells, often causing immune deficiency and AIDS-like
symptoms. These viruses and their hosts have provided researchers with
useful, albeit imperfect, models of the HIV disease process in people.


Graphic: Structure of HIV

The viral envelope

HIV has a diameter of 1/10,000 of a millimeter and is spherical in
shape. The outer coat of the virus, known as the viral envelope, is
composed of two layers of fatty molecules called lipids, taken from
the membrane of a human cell when a newly formed virus particle buds
from the cell. Evidence from NIAID-supported research indicates that
HIV may enter and exit cells through special areas of the cell
membrane known as “lipid rafts.” These rafts are high in cholesterol
and glycolipids and may provide a new target for blocking HIV.

Embedded in the viral envelope are proteins from the host cell, as
well as 72 copies (on average) of a complex HIV protein (frequently
called “spikes”) that protrudes through the surface of the virus
particle (virion). This protein, known as Env, consists of a cap made
of three molecules called glycoprotein (gp) 120, and a stem consisting
of three gp41 molecules that anchor the structure in the viral
envelope. Much of the research to develop a vaccine against HIV has
focused on these envelope proteins.

The viral core

Within the envelope of a mature HIV particle is a bullet-shaped core
or capsid, made of 2,000 copies of another viral protein, p24. The
capsid surrounds two single strands of HIV RNA, each of which has a
copy of the virus’s nine genes. Three of these genes, gag, pol, and
env , contain information needed to make structural proteins for new
virus particles. The env gene, for example, codes for a protein called
gp160 that is broken down by a viral enzyme to form gp120 and gp41,
the components of Env.

Six regulatory genes, tat, rev, nef, vif, vpr, and vpu, contain
information necessary to produce proteins that control the ability of
HIV to infect a cell, produce new copies of virus, or cause disease.
The protein encoded by nef, for instance, appears necessary for the
virus to replicate efficiently, and the vpu-encoded protein influences
the release of new virus particles from infected cells. Recently,
researchers discovered that Vif (the protein encoded by the vif gene)
interacts with an antiviral defense protein in host cells (APOBEC3G),
causing inactivation of the antiviral effect and enhancing HIV
replication. This interaction may serve as a new target for antiviral

The ends of each strand of HIV RNA contain an RNA sequence called the
long terminal repeat (LTR). Regions in the LTR act as switches to
control production of new viruses and can be triggered by proteins
from either HIV or the host cell.

The core of HIV also includes a protein called p7, the HIV
nucleocapsid protein. Three enzymes carry out later steps in the
virus’s life cycle: reverse transcriptase, integrase, and protease.
Another HIV protein called p17, or the HIV matrix protein, lies
between the viral core and the viral envelope.


Entry of HIV into cells

Infection typically begins when an HIV particle, which contains two
copies of the HIV RNA, encounters a cell with a surface molecule
called cluster designation 4 (CD4). Cells carrying this molecule are
known as CD4+ cells.

One or more of the virus’s gp120 molecules binds tightly to CD4
molecule(s) on the cell’s surface. The binding of gp120 to CD4 results
in a conformational change in the gp120 molecule allowing it to bind
to a second molecule on the cell surface known as a co-receptor. The
envelope of the virus and the cell membrane then fuse, leading to
entry of the virus into the cell. The gp41 of the envelope is critical
to the fusion process. Drugs that block either the binding or the
fusion process are being developed and tested in clinical trials. The
Food and Drug Administration (FDA) has approved one of the so-called
fusion inhibitors, T20, for use in HIV-infected people.

Studies have identified multiple coreceptors for different types of
HIV strains. These coreceptors are promising targets for new anti-HIV
drugs, some of which are now being tested in preclinical and clinical
studies. Agents that block the co-receptors are showing particular
promise as potential microbicides that could be used in gels or creams
to prevent HIV transmission. In the early stage of HIV disease, most
people harbor viruses that use, in addition to CD4, a receptor called
CCR5 to enter their target cells. With disease progression, the
spectrum of co-receptor usage expands in approximately 50 percent of
patients to include other receptors, notably a molecule called CXCR4.
Virus that uses CCR5 is called R5 HIV and virus that uses CXCR4 is
called X4 HIV.

Although CD4+ T cells appear to be the main targets of HIV, other
immune system cells with and without CD4 molecules on their surfaces
are infected as well. Among these are long-lived cells called
monocytes and macrophages , which apparently can harbor large
quantities of the virus without being killed, thus acting as
reservoirs of HIV. CD4+ T cells also serve as important reservoirs of
HIV; a small proportion of these cells harbor HIV in a stable,
inactive form. Normal immune processes may activate these cells,
resulting in the production of new HIV virions.

Cell-to-cell spread of HIV also can occur through the CD4-mediated
fusion of an infected cell with an uninfected cell.

Replication Cycle of HIV

Reverse transcription

In the cytoplasm of the cell, HIV reverse transcriptase converts viral
RNA into DNA, the nucleic acid form in which the cell carries its
genes. Fifteen of the 26 antiviral drugs approved in the United States
for treating people with HIV infection work by interfering with this
stage of the viral life cycle.


The newly made HIV DNA moves to the cell’s nucleus, where it is
spliced into the host’s DNA with the help of HIV integrase. HIV DNA
that enters the DNA of the cell is called a provirus. Several drugs
that target the integrase enzyme are in the early stages of
development and are being investigated for their potential as
antiretroviral agents.


For a provirus to produce new viruses, RNA copies must be made that
can be read by the host cell’s protein-making machinery. These copies
are called messenger RNA (mRNA), and production of mRNA is called
transcription, a process that involves the host cell’s own enzymes.
Viral genes in concert with the cellular machinery control this
process; the tat gene, for example, encodes a protein that accelerates
transcription. Genomic RNA is also transcribed for later incorporation
in the budding virion (see below).

Cytokines, proteins involved in the normal regulation of the immune
response, also may regulate transcription. Molecules such as tumor
necrosis factor (TNF)-alpha and interleukin (IL)-6, secreted in
elevated levels by the cells of HIV-infected people, may help to
activate HIV proviruses. Other infections, by organisms such as
Mycobacterium tuberculosis , also may enhance transcription by
inducing the secretion of cytokines.


After HIV mRNA is processed in the cell’s nucleus, it is transported
to the cytoplasm. HIV proteins are critical to this process; for
example, a protein encoded by the rev gene allows mRNA encoding HIV
structural proteins to be transferred from the nucleus to the
cytoplasm. Without the rev protein, structural proteins are not made.
In the cytoplasm, the virus co-opts the cell’s protein-making
machinery—including structures called ribosomes—to make long chains of
viral proteins and enzymes, using HIV mRNA as a template. This process
is called translation.

Assembly and budding

Newly made HIV core proteins, enzymes, and genomic RNA gather inside
the cell and an immature viral particle forms and buds off from the
cell, acquiring an envelope that includes both cellular and HIV
proteins from the cell membrane. During this part of the viral life
cycle, the core of the virus is immature and the virus is not yet
infectious. The long chains of proteins and enzymes that make up the
immature viral core are now cut into smaller pieces by a viral enzyme
called protease.

This step results in infectious viral particles. Drugs called protease
inhibitors interfere with this step of the viral life cycle. FDA has
approved eight such drugs—saquinavir, ritonavir, indinavir,
amprenavir, nelfinavir, fosamprenavir, atazanavir, and lopinavir—for
marketing in the United States. Recently, an HIV inhibitor that
targets a unique step in the viral life cycle, very late in the
process of viral maturation, has been identified and is currently
undergoing further development.

Recently, researchers have discovered that virus budding from the host
cell is much more complex than previously thought. Binding between the
HIV Gag protein and molecules in the cell directs the accumulation of
HIV components in special intracellular sacks, called multivesicular
bodies (MVB), that normally function to carry proteins out of the
cell. In this way, HIV actively hitch-hikes out of the cell in the MVB
by hijacking normal cell machinery and mechanisms. Discovery of this
budding pathway has revealed several potential points for intervening
in the viral replication cycle.


Among adults, HIV is spread most commonly during sexual intercourse
with an infected partner. During intercourse, the virus can enter the
body through the mucosal linings of the vagina, vulva, penis, or
rectum or, rarely, via the mouth and possibly the upper
gastrointestinal tract after oral sex. The likelihood of transmission
is increased by factors that may damage these linings, especially
other sexually transmitted infections that cause ulcers or

Research suggests that immune system cells of the dendritic cell type,
which live in the mucosa, may begin the infection process after sexual
exposure by binding to and carrying the virus from the site of
infection to the lymph nodes where other immune system cells become
infected. A molecule on the surface of dendritic cells, DC-SIGN, may
be critical for this transmission process.

HIV also can be transmitted by contact with infected blood, most often
by the sharing of needles or syringes contaminated with minute
quantities of blood containing the virus. The risk of acquiring HIV
from blood transfusions is extremely small in the United States, as
all blood products in this country are screened routinely for evidence
of the virus.

Almost all HIV-infected children in the United States get the virus
from their mothers before or during birth. In the United States,
approximately 25 percent of pregnant HIV-infected women not receiving
antiretroviral therapy have passed on the virus to their babies. In
1994, researchers showed that a specific regimen of the drug AZT
(zidovudine) can reduce the risk of transmission of HIV from mother to
baby by two-thirds. The use of combinations of antiretroviral drugs
and simpler drug regimens has further reduced the rate of
mother-to-child HIV transmission in the United States.

In developing countries, cheap and simple antiviral drug regimens have
been proven to significantly reduce mother-to-child transmission at
birth in resource-poor settings. Unfortunately, the virus also may be
transmitted from an HIV-infected mother to her infant via
breastfeeding. Moreover, due to the use of medicines to prevent
transmission at delivery, breastfeeding may become the most common
mode of HIV infection in infants. Thus, development of affordable
alternatives to breastfeeding is greatly needed.


Once it enters the body, HIV infects a large number of CD4+ cells and
replicates rapidly. During this acute or primary phase of infection,
the blood contains many viral particles that spread throughout the
body, seeding various organs, particularly the lymphoid organs .

Two to 4 weeks after exposure to the virus, up to 70 percent of
HIV-infected people suffer flu-like symptoms related to the acute
infection. Their immune system fights back with killer T cells (CD8+ T
cells) and B-cell-produced antibodies , which dramatically reduce HIV
levels. A person’s CD4+ T cell count may rebound somewhat and even
approach its original level. A person may then remain free of
HIV-related symptoms for years despite continuous replication of HIV
in the lymphoid organs that had been seeded during the acute phase of

One reason that HIV is unique is the fact that despite the body’s
aggressive immune responses, which are sufficient to clear most viral
infections, some HIV invariably escapes. This is due in large part to
the high rate of mutations that occur during the process of HIV
replication. Even when the virus does not avoid the immune system by
mutating, the body’s best soldiers in the fight against HIV—certain
subsets of killer T cells that recognize HIV—may be depleted or become

In addition, early in the course of HIV infection, people may lose
HIV-specific CD4+ T cell responses that normally slow the replication
of viruses. Such responses include the secretion of interferons and
other antiviral factors, and the orchestration of CD8+ T cells.

Finally, the virus may hide within the chromosomes of an infected cell
and be shielded from surveillance by the immune system. Such cells can
be considered as a latent reservoir of the virus. Because the
antiviral agents currently in our therapeutic arsenal attack actively
replicating virus, they are not effective against hidden, inactive
viral DNA (so-called provirus). New strategies to purge this latent
reservoir of HIV have become one of the major goals for current
research efforts.


Among people enrolled in large epidemiologic studies in Western
countries, the median time from infection with HIV to the development
of AIDS-related symptoms has been approximately 10 to 12 years in the
absence of antiretroviral therapy. Researchers, however, have observed
a wide variation in disease progression. Approximately 10 percent of
HIV-infected people in these studies have progressed to AIDS within
the first 2 to 3 years following infection, while up to 5 percent of
individuals in the studies have stable CD4+ T cell counts and no
symptoms even after 12 or more years.

Factors such as age or genetic differences among individuals, the
level of virulence of an individual strain of virus, and co-infection
with other microbes may influence the rate and severity of disease
progression. Drugs that fight the infections associated with AIDS have
improved and prolonged the lives of HIV-infected people by preventing
or treating conditions such as Pneumocystis carinii pneumonia,
cytomegalovirus disease, and diseases caused by a number of fungi.

HIV co-receptors and disease progression

Recent research has shown that most infecting strains of HIV use a
co-receptor molecule called CCR5, in addition to the CD4 molecule, to
enter certain of its target cells. HIV-infected people with a specific
mutation in one of their two copies of the gene for this receptor may
have a slower disease course than people with two normal copies of the
gene. Rare individuals with two mutant copies of the CCR5 gene appear,
in most cases, to be completely protected from HIV infection.
Mutations in the gene for other HIV co-receptors also may influence
the rate of disease progression.

Viral burden and disease progression

Numerous studies show that people with high levels of HIV in their
bloodstream are more likely to develop new AIDS-related symptoms or
die than those with lower levels of virus. For instance, in the
Multicenter AIDS Cohort Study (MACS), investigators showed that the
level of HIV in an untreated person’s plasma 6 months to a year after
infection—the so-called viral “set point”—is highly predictive of the
rate of disease progression; that is, patients with high levels of
virus are much more likely to get sicker faster than those with low
levels of virus. The MACS and other studies have provided the
rationale for providing aggressive antiretroviral therapy to
HIV-infected people, as well as for routinely using newly available
blood tests to measure viral load when initiating, monitoring, and
modifying anti-HIV therapy.

Potent combinations of three or more anti-HIV drugs known as highly
active antiretroviral therapy, or HAART, can reduce a person’s “viral
burden” (amount of virus in the circulating blood) to very low levels
and in many cases delay the progression of HIV disease for prolonged
periods. Before the introduction of HAART therapy, 85 percent of
patients survived an average of 3 years following AIDS diagnosis.
Today, 95 percent of patients who start therapy before they get AIDS
survive on average 3 years following their first AIDS diagnosis. For
those who start HAART after their first AIDS event, survival is still
very high at 85 percent, averaging 3 years after AIDS diagnosis.

Antiretroviral regimens, however, have yet to completely and
permanently suppress the virus in HIV-infected people. Recent studies
have shown that, in addition to the latent HIV reservoir discussed
above, HIV persists in a replication-competent form in resting CD4+ T
cells even in people receiving aggressive antiretroviral therapy who
have no readily detectable HIV in their blood. Investigators around
the world are working to develop the next generation of anti-HIV drugs
that can stop HIV, even in these biological scenarios.

A treatment goal, along with reduction of viral burden, is the
reconstitution of the person’s immune system, which may have become
sufficiently damaged that it cannot replenish itself. Various
strategies for assisting the immune system in this regard are being
tested in clinical trials in tandem with HAART, such as the Evaluation
of Subcutaneous Proleukin in a Randomized International Trial (ESPRIT)
trial exploring the effects of the T cell growth factor, IL-2.


Although HIV-infected people often show an extended period of clinical
latency with little evidence of disease, the virus is never truly
completely latent although individual cells may be latently infected.
Researchers have shown that even early in disease, HIV actively
replicates within the lymph nodes and related organs, where large
amounts of virus become trapped in networks of specialized cells with
long, tentacle-like extensions. These cells are called follicular
dendritic cells (FDCs). FDCs are located in hot spots of immune
activity in lymphoid tissue called germinal centers. They act like
flypaper, trapping invading pathogens (including HIV) and holding them
until B cells come along to start an immune response.

Over a period of years, even when little virus is readily detectable
in the blood, significant amounts of virus accumulate in the lymphoid
tissue, both within infected cells and bound to FDCs. In and around
the germinal centers, numerous CD4+ T cells are probably activated by
the increased production of cytokines such as TNF-alpha and IL-6 by
immune system cells within the lymphoid tissue. Activation allows
uninfected cells to be more easily infected and increases replication
of HIV in already infected cells.

While greater quantities of certain cytokines such as TNF-alpha and
IL-6 are secreted during HIV infection, other cytokines with key roles
in the regulation of normal immune function may be secreted in
decreased amounts. For example, CD4+ T cells may lose their capacity
to produce IL-2, a cytokine that enhances the growth of other T cells
and helps to stimulate other cells' response to invaders. Infected
cells also have low levels of receptors for IL-2, which may reduce
their ability to respond to signals from other cells.

Breakdown of lymph node architecture

Ultimately, with chronic cell activation and secretion of inflammatory
cytokines, the fine and complex inner structure of the lymph node
breaks down and is replaced by scar tissue. Without this structure,
cells in the lymph node cannot communicate and the immune system
cannot function properly. Investigators also have reported recently
that this scarring reduces the ability of the immune system to
replenish itself following antiretroviral therapy that reduces the
viral burden.


CD8+ T cells are critically important in the immune response to HIV.
These cells attack and kill infected cells that are producing virus.
Thus, vaccine efforts are directed toward eliciting or enhancing these
killer T cells, as well as eliciting antibodies that will neutralize
the infectivity of HIV.

CD8+ T cells also appear to secrete soluble factors that suppress HIV
replication. Several molecules, including RANTES, MIP-1alpha,
MIP-1beta, and MDC appear to block HIV replication by occupying the
coreceptors necessary for many strains of HIV to enter their target
cells. There may be other immune system molecules—including the
so-called CD8 antiviral factor (CAF), the defensins (type of
antimicrobials), and others yet undiscovered—that can suppress HIV
replication to some degree.


HIV replicates rapidly; several billion new virus particles may be
produced every day. In addition, the HIV reverse transcriptase enzyme
makes many mistakes while making DNA copies from HIV RNA. As a
consequence, many variants or strains of HIV develop in a person, some
of which may escape destruction by antibodies or killer T cells.
Additionally, different strains of HIV can recombine to produce a wide
range of variants.

During the course of HIV disease, viral strains emerge in an infected
person that differ widely in their ability to infect and kill
different cell types, as well as in their rate of replication.
Scientists are investigating why strains of HIV from people with
advanced disease appear to be more virulent and infect more cell types
than strains obtained earlier from the same person. Part of the
explanation may be the expanded ability of the virus to use other
co-receptors, such as CXCR4.


Researchers around the world are studying how HIV destroys or disables
CD4+ T cells, and many think that a number of mechanisms may occur
simultaneously in an HIV-infected person. Data suggest that billions
of CD4+ T cells may be destroyed every day, eventually overwhelming
the immune system’s capacity to regenerate.

Direct cell killing

Infected CD4+ T cells may be killed directly when large amounts of
virus are produced and bud out from the cell surface, disrupting the
cell membrane, or when viral proteins and nucleic acids collect inside
the cell, interfering with cellular machinery.


Infected CD4+ T cells may be killed when the regulation of cell
function is distorted by HIV proteins, probably leading to cell
suicide by a process known as programmed cell death or apoptosis.
Recent reports indicate that apoptosis occurs to a greater extent in
HIV-infected people, both in their bloodstream and lymph nodes.
Apoptosis is closely associated with the aberrant cellular activation
seen in HIV disease.

Uninfected cells also may undergo apoptosis. Investigators have shown
in cell cultures that the HIV envelope alone or bound to antibodies
sends an inappropriate signal to CD4+ T cells causing them to undergo
apoptosis, even if not infected by HIV.

Innocent bystanders

Uninfected cells may die in an innocent bystander scenario: HIV
particles may bind to the cell surface, giving them the appearance of
an infected cell and marking them for destruction by killer T cells
after antibody attaches to the viral particle on the cell. This
process is called antibody-dependent cellular cytotoxicity.

Killer T cells also may mistakenly destroy uninfected cells that have
consumed HIV particles and that display HIV fragments on their
surfaces. Alternatively, because HIV envelope proteins bear some
resemblance to certain molecules that may appear on CD4+ T cells, the
body’s immune responses may mistakenly damage such cells as well.


Researchers have shown in cell cultures that CD4+ T cells can be
turned off by activation signals from HIV that leaves them unable to
respond to further immune stimulation. This inactivated state is known
as anergy.

Damage to precursor cells

Studies suggest that HIV also destroys precursor cells that mature to
have special immune functions, as well as the microenvironment of the
bone marrow and the thymus needed for developing such cells. These
organs probably lose the ability to regenerate, further compounding
the suppression of the immune system.


Although monocytes and macrophages can be infected by HIV, they appear
to be relatively resistant to being killed by the virus. These cells,
however, travel throughout the body and carry HIV to various organs,
including the brain, which may serve as a hiding place or “reservoir”
for the virus that may be relatively resistant to most anti-HIV drugs.

Neurologic manifestations of HIV disease are seen in up to 50 percent
of HIV-infected people, to varying degrees of severity. People
infected with HIV often experience

* Cognitive symptoms, including impaired short-term memory,
reduced concentration, and mental slowing
* Motor symptoms such as fine motor clumsiness or slowness,
tremor, and leg weakness
* Behavioral symptoms including apathy, social withdrawal,
irritability, depression, and personality change

More serious neurologic manifestations in HIV disease typically occur
in patients with high viral loads, generally when a person has
advanced HIV disease or AIDS.

Neurologic manifestations of HIV disease are the subject of many
research projects. Current evidence suggests that although nerve cells
do not become infected with HIV, supportive cells within the brain,
such as astrocytes and microglia (as well as monocyte/macrophages that
have migrated to the brain) can be infected with the virus.
Researchers postulate that infection of these cells can cause a
disruption of normal neurologic functions by altering cytokine levels,
by delivering aberrant signals, and by causing the release of toxic
products in the brain. The use of anti-HIV drugs frequently reduces
the severity of neurologic symptoms, but in many cases does not, for
reasons that are unclear. The impact of long-term therapy and
long-term HIV disease on neurologic function is also unknown and under
intensive study.


During a normal immune response, many parts of the immune system are
mobilized to fight an invader. CD4+ T cells, for instance, may quickly
multiply and increase their cytokine secretion, thereby signaling
other cells to perform their special functions. Scavenger cells called
macrophages may double in size and develop numerous organelles ,
including lysosomes that contain digestive enzymes used to process
ingested pathogens. Once the immune system clears the foreign antigen,
it returns to a relative state of quiescence.

Paradoxically, although it ultimately causes immune deficiency, HIV
disease for most of its course is characterized by immune system
hyperactivation, which has negative consequences. As noted above, HIV
replication and spread are much more efficient in activated CD4+
cells. Chronic immune system activation during HIV disease also may
result in a massive stimulation of B cells, impairing the ability of
these cells to make antibodies against other pathogens.

Chronic immune activation also can result in apoptosis, and an
increased production of cytokines that not only may increase HIV
replication but also have other deleterious effects. Increased levels
of TNF-alpha, for example, may be at least partly responsible for the
severe weight loss or wasting syndrome seen in many HIV-infected

The persistence of HIV and HIV replication plays an important role in
the chronic state of immune activation seen in HIV-infected people. In
addition, researchers have shown that infections with other organisms
activate immune system cells and increase production of the virus in
HIV-infected people. Chronic immune activation due to persistent
infections, or the cumulative effects of multiple episodes of immune
activation and bursts of virus production, likely contribute to the
progression of HIV disease.


The clinical spectrum of disease among people with HIV has changed
dramatically in the era of HAART. NIAID and its grantees are actively
studying the new clinical syndrome of disease among persons on long
term-therapy. Research is concentrating on the impact of HIV over the
long term, the toxicity of the medicines used to control HIV, and the
effects of aging on HIV disease progression. People with HIV have a
variety of conditions including diabetes, heart disease,
neurocognitive decline, and cancers that may, or may not, be directly
due to HIV or its treatment. Long-term studies of people with HIV in
the United States and abroad are underway.


NIAID-supported scientists conduct research on HIV pathogenesis in
laboratories on the campus of the National Institutes of Health (NIH)
in Bethesda, Maryland; at the Institute’s Rocky Mountain Laboratories
in Hamilton, Montana; and at universities and medical centers in the
United States and abroad.

An NIAID-supported resource, the NIH AIDS Research and Reference
Reagent Program , in collaboration with the World Health Organization,
provides critically needed AIDS-related research materials free to
qualified researchers around the world.

The NIH Centers for AIDS Research , supported by NIAID in
collaboration with six other NIH Institutes, fosters and facilitates
development of infrastructure and interdisciplinary collaboration of
HIV researchers at major medical and research centers across the
United States.

In addition, the Institute convenes groups of investigators and
advisory committees to exchange scientific information, clarify
research priorities, and bring research needs and opportunities to the
attention of the scientific community.


antibodies - infection-fighting protein molecules in blood or
secretory fluids that tag, neutralize, and help destroy pathogenic
microorganisms such as viruses.

apoptosis - cellular suicide, also known as programmed cell death. HIV
may induce apoptosis in both infected and uninfected immune system

B cells - white blood cells of the immune system that produce
infection-fighting proteins called antibodies.

CD4+ T cells - white blood cells that orchestrate the immune response,
signaling other cells in the immune system to perform their special
functions. Also known as T helper cells, these cells are killed or
disabled during HIV infection.

CD8+ T cells - white blood cells that kill cells infected with HIV or
other viruses, or transformed by cancer. These cells also secrete
soluble molecules that may suppress HIV without killing infected cells

cytokines - proteins used for communication by cells of the immune
system. Central to the normal regulation of the immune response.

cytoplasm - the living matter within a cell.

dendritic cells - immune system cells with long, tentacle-like
branches. Some of these are specialized cells at the mucosa that may
bind to HIV following sexual exposure and carry the virus from the
site of infection to the lymph nodes. See also follicular dendritic

enzyme - a protein that accelerates a specific chemical reaction
without altering itself.

follicular dendritic cells (FDCs) - cells found in the germinal
centers (B cell areas) of lymphoid organs. FDCs have thread-like
tentacles that form a web-like network to trap invaders and present
them to B cells, which then make antibodies to attack the invaders.

germinal centers - structures within lymphoid tissues that contain
FDCs and B cells, and in which immune responses are initiated.

gp41 - glycoprotein 41, a protein embedded in the outer envelope of
HIV. Plays a key role in HIV’s infection of CD4+ T cells by
facilitating the fusion of the viral and cell membranes.

gp120 - glycoprotein 120, a protein that protrudes from the surface of
HIV and binds to CD4+ T cells.

gp160 - glycoprotein 160, an HIV precursor protein that is cleaved by
the HIV protease enzyme into gp41 and gp120.

immune deficiency - the inability of the immune system to work
properly, resulting in susceptibility to disease.

immunosuppression - immune system response to foreign invaders such as
HIV is reduced

integrase - an HIV enzyme used by the virus to integrate its genetic
material into the host cell's DNA.

Kaposi’s sarcoma - a type of cancer characterized by abnormal growths
of blood vessels that develop into purplish or brown lesions.

killer T cells - see CD8+ T cells.

lentivirus - “slow” virus characterized by a long interval between
infection and the onset of symptoms. HIV is a lentivirus as is the
simian immunodeficiency virus (SIV), which infects nonhuman primates.

LTR - long terminal repeat, the RNA sequences repeated at both ends of
HIV’s genetic material. These regulatory switches may help control
viral transcription.

lymphoid organs - include tonsils, adenoids, lymph nodes, spleen, and
other tissues. Act as the body’s filtering system, trapping invaders
and presenting them to squadrons of immune cells that congregate

macrophage - a large immune system cell that devours invading
pathogens and other intruders. Stimulates other immune system cells by
presenting them with small pieces of the invaders.

microbes - microscopic living organisms, including viruses, bacteria,
fungi, and protozoa.

monocyte - a circulating white blood cell that develops into a
macrophage when it enters tissues.

opportunistic infection - an illness caused by an organism that
usually does not cause disease in a person with a normal immune
system. People with advanced HIV infection suffer opportunistic
infections of the lungs, brain, eyes, and other organs.

organelles - small structures inside a cell, generally bounded by

pathogenesis - the production or development of a disease. May be
influenced by many factors, including the infecting microbe and the
host’s immune response.

pathogens - disease-causing organisms.

protease - an HIV enzyme used to cut large HIV proteins into smaller
ones needed for the assembly of an infectious virus particle.

provirus - DNA of a virus, such as HIV, that has been integrated into
the genes of a host cell.

replicate: process by which a virus makes copies of itself.

retrovirus - HIV and other viruses that carry their genetic material
in the form of RNA and that have the enzyme reverse transcriptase.

reverse transcriptase - the enzyme produced by HIV and other
retroviruses that allows them to synthesize DNA from their RNA.

NIAID is a component of the National Institutes of Health (NIH),
which is an agency of the Department of Health and Human Services.
NIAID supports basic and applied research to prevent, diagnose, and
treat infectious and immune-mediated illnesses, including HIV/AIDS and
other sexually transmitted diseases, illness from potential agents of
bioterrorism, tuberculosis, malaria, autoimmune disorders, asthma and

News releases, fact sheets and other NIAID-related materials are
available on the NIAID Web site at http://www.niaid.nih.gov.

Prepared by:
Office of Communications and Public Liaison
National Institute of Allergy and Infectious Diseases
National Institutes of Health
Bethesda, MD 20892
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medicine forum addict

Joined: 02 Apr 2006
Posts: 93

PostPosted: Sat Jul 15, 2006 9:00 am    Post subject: Re: AIDS Reply with quote

This is "old news," TC. I'd suggest people read posts at
http://groups.msn.com/aidsmythexposed/general.msnw or read some of the
essays at www.theperthgroup.com for more up to date information.
People like Mr. Carter attack Peter Duesberg, who appears to have been
wrong on several key points, but they act as if he is the only "AIDS
dissident" in the world. I explain some of this on my web site,

For example, a point I make is that "Koch's Postulates" violates the
scientific method, so it is quite irrelevant to talk about it in any
scientific context. What they do to get around this is to say things
like, "well, we really don't know why there are exceptions, but we will
have to leave that up to future generations - however, now we have
enough evidence to proceed as we have been." Would this be tolerated
if one in every 100 bridges collapsed within a few weeks of completion?
Think of how many bridges have been built even on short segments of
highways. And keep in mind that engineering is an applied science,
whereas I'm am talking about the higher standard of theoretical
science, as well as the Hippocratic Oath,which says to do no harm (the
"HIV medication" can do tremendous harm - destroying livers quickly,
for instance).

One thing that is interesting here is that Mr. Carter finally cited
something from the literature. Unfortunately, what it demonstrates is
the lack of evidence. Someone, the powers that be in the biomedical
establishment think that if a lack of evidence sounds "scientific,"
then it can substitute as evidence. Basically, they talk about things
that are correlated, but not cytotoxic effects that are actually
observed. Attempts have been made to do this, and the technology is
capable, yet it has never been detected. Moreover, and more
egregiously (at least to me) is that there are other scientific
explanations for this (explained on my web site, though unlike this
piece of nonsense, I actually supply ample citations from the
literature). In science, when at least two explanations are possible,
one is supposed to do controlled experiments to see which one appears
to be correct. This has not been done with "AIDS." Instead, "virus
hunters" jumped in and simply declared that a virus was present and
doing the damage. In reality, and again as I explain on my web site
(with citations), viruses are "deadly" because they provoke a dangerous
inflammatory response, not because of a direct, cell killing effect.
And this happens quickly - hours or days, not after years of good
health. In order for a virus to do this, it would have to be "turned
on" by something else, and so a co-factor would have to be present.
Otherwise, if the virus was doing something nasty for all those years,
it would have been detected already, over 20 years since the Gallo
press conference.

There are also misleading statements in this entry quoted by Mr.
Carter. I don't have the time to speak on every one, but let us take
the following simple one:

"HIV belongs to a subgroup of retroviruses..."

However, retroviruses are of a certain size and shape, and despite
numerous attempts to do so, nothing of the right size and shape has
been found in any tissue of anyone said to be infected with "HIV" or
dying of "AIDS," despite several professional attempts. It is now
well-known that excessive antigenic exposure and/or oxidative stress
can create the kind of symptoms deemed to be signs of "immune system
collapse" in "AIDS patients." Thus, the proper thing to do is to
experiment, to see if those said to be "dying of AIDS" are peope who
are exposed to a great deal of antigens and/or oxidative stress. This
has never been done. But what's worse, if it was done, and if it was
found that such people die of "AIDS," despite "testing negative for
HIV" before being monitored by the researchers (and not engaging in any
"risk" activities afterwards), the powers that be would disallow the
results, because they claim that only "HIV" can cause "AIDS." This
goes beyond a violation of the scientific method. It is a violation of
basic logic. For those who don't know, "AIDS" is technically a
clinical syndrome (CS), which is used when a cause is not known but
when symptoms appear to be related in some way. Over time, the CS
should be narrowed, and possibly several CSs should replace the first
one. The other possibility is that the exact cause of the CS becomes
known, and then the CS can be abandoned. Usually, it will then be
called X disease instead. With "HIV/AIDS," all of this has been tossed
out the proverbial window. The CS has been widened, despite more being
known now, and it's been widened in a way that makes no sense, now
including cervical cancer, for instance. Most of us realize that there
is no way to reason with a stark raving mad lunatic, and what the
"HIV/AIDS" experts have done is to enshrine a certain kind of insanity
in a way that is antithetical to the most basic tenets of science.

I will conclude here by quoting a very useful, hypothetical dialogue
between doctor and patient, reminiscent of Galileo's famous work. The
source of this is: http://www.theperthgroup.com/FAQ/question8.html


Doctor: I am sorry to have to tell you but your antibody test has come
back positive.

Patient: You're telling me I have HIV?

Dr: I'm afraid so.

P: Couldn't the test be mistaken?

Dr: Unfortunately not. The tests we use are extremely sensitive and
specific. I have never known them to make a mistake.

P: Doctor can you please explain how this particular test can be so
accurate? And how it actually works?

Dr: Certainly. In simple terms the test has detected some antibodies
to HIV in your blood. The only way you can get those antibodies is to
come into contact with HIV.

P: When you say the antibodies are 'to' HIV, what do you mean?

Dr: I mean they are directed against HIV. When your body came into
contact with HIV it registered the HIV proteins as something foreign.
As a result your immune system was switched on to produce a set of
antibodies which specifically combine with these proteins.

P: How do you know these antibodies are actually there? In my body?

Dr : Because when we mix your blood with the proteins in the antibody
test kits there's a reaction.

P: How do you know there's a reaction?

Dr: Because when we add your serum to a solution containing the test
kit proteins the solution changes colour. We can see that and we can
even measure the amount of reaction by the amount of colour change. We
get out a number which makes it quite objective.

P: And when you say 'reaction' do you mean a chemical reaction?

P: Yes. There is a chemical reaction. That's because the antibodies
in your blood recognise the HIV proteins. The shape of the antibodies
and protein molecules are complementary. They fit together perfectly.
Like a lock and key. That's what specific means.

P: But this is not a test for the actual virus is it? The virus
particles? You haven't found those in my body?

Dr: No it's not the actual virus. It's an indirect test. As I
explained, it's a test that looks for antibodies that are
manufactured in response to the presence of the virus proteins.
That's why we call them HIV antibodies. But the virus is there all
right. There's no other reason why your body would produce such

P: So if you looked you could also find the virus particles?

Dr: Maybe and maybe not. Not necessarily in your blood. That would be
very hard to do because to see them you need millions and millions of
particles. In fact no one has ever managed to find HIV particles in a
patient's blood. But we could use your blood to culture the virus.
Outside your body. Or we could do the same thing from a small piece of
lymph node for example. But these kind of tests are technically
demanding. And expensive. And quite unnecessary.

P: Where do you get the HIV proteins from?

Dr: From HIV. They form the major part of the HIV particle.

P: I presume these proteins don't occur anywhere else then?

Dr: No. They belong to HIV.

P: And nothing else you know of could induce my immune system to make
these antibodies?

Dr: The way the tests have been refined and interpreted, no.

P: So you're sure my body has this virus in it?

Dr: As sure as anyone can be.

A week later.

Patient: Doctor I've done a literature search and I've looked up
some articles in the University library. I've made you some copies
as well.

Dr: I assume you have a few more questions then? About what we
discussed last time? I know it's hard coming to grips with something
like this.

P: To be perfectly honest I'm confused. I'd really like to know
what you think. For instance, last week you told me the HIV proteins,
the ones used to test my blood for antibodies, don't occur anywhere
else except in HIV.

Dr : That's right.

P: Here's a paper I found. It's called "HIV proteins in normal
human placentae.1 It's written by a group of scientists who tested
tissue from the placentas of several healthy, pregnant women using
antibodies directed against four of the HIV proteins. They found three
HIV proteins in women who are not infected with HIV. They were p18,
p24 and p120. And here's another article. This one's called
"Monoclonal antibodies to the human immunodeficiency virus p18
protein cross-react with normal human tissues".2 In this paper the
HIV p18 protein was found in the thymus and tonsils and brains of
people who are not infected with HIV. Are you familiar with these

Dr: I'm sorry I've not seen these before. And I would have to
read them before passing comment.

P: You might have to read quite a few. Here's another paper where
blood from five patients who were HIV negative was cultured and again
the p24 protein was found. I've got another paper for p32. And
several other papers confirming what I've already said about the
others.1-7 8 9-16 I'm no expert but it seems to me if the
antibodies used in these experiments are the same antibodies that are
in AIDS patients, or in me for instance, and they specifically
recognise the HIV proteins, they should not register anything in HIV
negative people's blood or tissues. Doctor what is going on?

Dr: You're jumping to the wrong conclusion. The HIV proteins are
not there. It only looks that way. As your second paper says in its
title, the antibodies cross-react with some normal human proteins.
That occur in brain for example.

P: But aren't the antibodies they used in these experiments meant to
be specific? Don't they recognise HIV and nothing else but HIV?

Dr: When I explained the test to you last week I did say I was giving
you a simplified version.

P: All right but how come these antibodies react in normal people? If
there's not a simple answer is there a complicated answer?

Dr: What these papers are describing is not strange or mysterious. And
it's not a secret. The problem is that antibodies aren't always
exactly 100% specific. Sometimes they can and will react with other
things besides what they're meant for. That's what cross-react

P: So you're saying that HIV antibodies can react with things other
than HIV?

Dr: Yes.

P: So if an antibody reacts with something that's not proof it's
directed against that something?

Dr: It may not be.

P: Are HIV antibodies the only antibodies that can cross-react?

Dr: No. In theory it's possible for any antibody to cross-react.
It's not a property confined to one type of antibody.

P: Well if HIV antibodies can cross-react with proteins which are not
HIV, like in the brain for example, then why can't non-HIV antibodies
cross-react with the proteins you say do come from HIV?

Dr: In theory they can.

P: What about in practice?

Dr: Yes they can. That is reported in the literature.

P: So how do you know the antibodies in my blood, the ones that react
in my test, are caused by HIV and not by something else?

A week later.

Dr: I understand this must be causing you considerable distress. So
I've set aside some extra time to fully go over these tests.

P: I appreciate that doctor. We were talking about cross-reactions.

Dr: I remember. OK. And let me know if I lose you in what I am about
to say. Sometimes antibodies to one protein do react with another,
different protein. That happens because the fit between the bit of the
protein the antibody reacts with, and the antibody itself, although not
100% perfect, is still good enough for a reaction to take place.

P: I understand.

Dr: Now back in 1985, when the HIV tests were being designed, when HIV
testing was in its infancy, it was discovered there are people who are
not infected with HIV who have antibodies that react with one or even a
couple of the HIV proteins.

P: But that wasn't an infection?

Dr: No, that was cross-reactions.

P: How many people does that affect doctor?

Dr It varies depending on what papers you read. But in one of the
types of test we do, it's called the Western blot, can be as high as
25%. It's certainly at least 15%. The 25% figure is from Australia.
From studies of healthy blood donors.

P: And these people definitely are not infected with HIV?

Dr: No they're not.

P: How do you know they're not? How do you know they haven't got
the real HIV antibodies?

Dr: Because these people don't belong to a risk group. And
they're healthy and they stay healthy. They don't go on to develop
AIDS. And when they donate blood the recipients don't develop AIDS

P: And 25% of the population couldn't possibly be infected with HIV?

Dr: Exactly. If they were I can't imagine how many hospitals we
would need to treat them all.

P: And for HIV to get that common life would have to be one continuous

Dr: A very good point.

P: But these antibodies must have come from somewhere?

Dr: That's true. Something must be responsible. And it's often
hard to know exactly what. Although it really isn't important to know
that. Perhaps they're caused by some other illness or some exposure
to something in the environment. But whatever it is, it's not HIV.

P: I understand.

Dr: Now, I said before, we do have a way to sort out true HIV
antibodies from all the others.

P: Yes I remember your saying that. The wheat from the chaff.

Dr: That's a good analogy. Let me tell you what happens. When we
first test you we do what's called an ELISA test. That is known as a
screening test. In the ELISA we test your blood against all the
proteins from HIV. All mixed up together. That's about ten proteins
by the way. So we have all the proteins in one test-tube and then we
add a few drops of your blood sample. Minus the red blood cells of
course. Otherwise we wouldn't see any colour except red. So we add
the serum, where the antibodies are dissolved, not the whole blood. If
there's a reaction the solution changes colour. We can see that. As
I said before, we measure the amount of the reaction by measuring the
passage of a light beam through the solution.

P: With the spectrophotometer?

Dr: Yes. You've obviously been doing a lot of study.

P: I also did two years of chemistry as an undergraduate.

Dr: OK. But there's a problem with the ELISA. It's not that
specific. Or at least it's not specific enough. We can't do just
one ELISA test then look you in the eye and say you're infected.
That would not be considered best practice.

P: So why do you use this test?

Dr: Because it is the most sensitive antibody test. By that I mean
it's guaranteed to pick up every HIV single antibody anyone could
ever have-but at a price. It also has a tendency to pick up non-HIV
antibodies as well. To use your analogy, it picks up all the wheat OK,
every single grain, but along with that some of the chaff. By that I
mean antibodies which are not HIV.

P: I still don't understand why you use it.

Dr : We use it to screen people. The way it works is this: If the
ELISA is negative it hasn't picked up any antibodies. HIV or
non-HIV. So the person is not infected. In that case that's as far
as we need to go. So it's a very useful first up test. It's used
a lot for donating blood. Most people who want to donate blood are
negative on the ELISA. In fact most people period are ELISA negative.
End of story.

P: And what if a blood donor is positive?

Dr: Then we have to dig deeper. But for the blood bank it means they
know straight away they can or can't use that person's blood.
It's quick and easy.

P: But what happens to the blood donor who is positive on the ELISA?

Dr: If the blood bank find a positive they hand over the case to an
approved laboratory for running further tests. Such as our laboratory.
In fact that's the law in this country. Not just any person or
laboratory is allowed to do the further tests. Then it's really no
different from what happened in your case. We dig deeper by doing
another test. A test which is different from the ELISA. In most parts
of the world the second type of test is the Western blot. The
difference is that in the Western blot the ten HIV proteins are not
mixed up together. They have been separated from each another along a
paper strip about half a centimeter wide. That way we can identify
precisely which HIV proteins are reacting. Or if you like, we can tell
which antibodies you have to which HIV proteins.

P: How do you read the Western blot?

Dr: By eye. Every place where an antibody reacts with one of the HIV
proteins the strip changes colour. So you end up with a series of
coloured dots along the strip. We call those bands. The lab
technician looks at the strip and reports the names of the bands that
light up. Each band is named with a 'p' for protein and then a
number which is its molecular weight in thousands. I think you've
already found that out.

P: How does the number of bands determine whether someone is infected
or not?

Dr: Well you might have one band or you might have ten bands. If you
only have a couple of bands then you're almost certainly dealing with
cross-reactions. But if you have four or more your test is positive
and you are infected. Or of course you might have no bands which means
you are definitely negative and not infected.

P: So the Western blot is used to work out whether the ELISA is right
or wrong?

Dr : Yes. We say the Western blot is a 'confirmatory' test.

P: And knowing which bands a person has distinguishes real antibodies
from cross-reactions?

Dr: Yes. We know that HIV antibodies cause particular patterns of
bands to show up. Kind of like a Lotto ticket. Certain combinations
invariably mean a prize and others don't.

P: What does my Western blot test show? Which antibody bands do I

Dr: You have antibodies to p41, p24, p32 and p18. That's four bands
and it's also one of the several possible band patterns that makes a
positive test.

P: I still don't understand how you can know that some band patterns
are caused by HIV and others are not.

Dr: OK. Tell me what you don't understand.

P: Last week I asked how you know blood donors who have one or two
antibodies aren't infected with HIV. You told me it's because they
aren't sick or in a risk group.

Dr: And they don't go on to develop AIDS.

P: OK. But if I had only one band on the Western blot you'd say
that was not an HIV antibody?

Dr : You can have up to three bands not caused by HIV antibodies. Or
at least the chances are very slim. Of course it might also be that
you haven't produced all your antibodies yet. It's early days.
You are on the way but your infection was only a few weeks ago. In
some people it can take a couple of months for all their antibodies to
show up. The bands don't appear simultaneously. It's called the
window period.

P: I could have as many as three antibodies and not be infected?

Dr: Yes. As many as that. And as long as you don't get any more.

P: So I could have three bands and not have HIV while the next patient
you see today could have the same three plus one extra band. And that
extra one produces a pattern you say is caused by 'real' HIV

Dr: That's quite possible.

P: Then the three bands he shares with me must be real HIV for him but
not for me. So that extra band makes all the difference?

Dr: Precisely.

P: I don't get it. Why should just one extra band be 'real'
when the others on their own aren't? How can a number or combination
determine which antibodies are real and which aren't? I mean if you
have three pieces of fruit that aren't apples and then you add a
fourth that is an apple, does that make four apples?

Dr: I agree but we have evidence. I said it before. We know which
band patterns are caused by HIV because we've analysed which
groupings of bands distinguish people with AIDS from those who remain
healthy. It's really not that difficult.

A week later

P: I've been thinking about what you told me. I'm sorry but I
still have problems.

Dr : Well we better keep talking. Fire away.

P: I have a cousin in the US who works for a biotechnology company. He
sells antibody test kits to several New York hospitals. He faxed me a
packet insert for the ELISA and Western blot. One of each. Which I
read last week.

Dr : And what did they say?

P: They confirmed what you said. With the ELISA you can distinguish
most people with AIDS from healthy people. If you use a combination as
you said, an ELISA followed by a Western blot, the distinction is
almost perfect.

Dr: Then doesn't that put the matter to rest?

P: Maybe. Maybe not.

Dr What's the difficulty?

P: The biotechnology companies want their tests to be highly specific.
In other words, they don't want their tests to react in someone
who's not infected with HIV. And neither I guess do the doctors.
And certainly not the patients. So, as you said, they try their tests
out on healthy blood donors. To see how good they are. They assume,
quite rightly I suppose, those sorts of people don't have much chance
of getting AIDS or being infected with HIV.

Dr : That's right. They're extremely unlikely to be infected with
HIV. That's been proven time and time again by millions of tests at
the blood banks.

P: Yes doctor but when the biotechnology companies test their tests on
blood donors they go further. They actually define the blood donors as
not infected. The World Health Organisation does the same thing.

Dr: That's correct.

P: Well that's one of the problems. When I read about healthy blood
donors, not being in a risk group and all the rest, I asked myself, who
are these people? Where do they live? What kind of people are they?
What are their habits? Where do they hang out? And you know who it
reminded me of?

Dr: No.

P: It reminded me of me. I'm healthy. My friends regularly tell me
how well I look. I only got HIV tested because I need life insurance.
I'm not gay, I'm not a haemophiliac, I'm never been a drug taker.
I've not been promiscuous. I haven't been an angel but since
getting married my only sexual partner has been my wife. And because
we were about to start a family, a couple of months ago, unbeknown to
me, my wife had an HIV test. And she's negative.

Dr: What point are you making?

P: Doctor I could easily be in a group of people the manufacturers of
antibody tests use to determine how accurate their tests are. And when
they tested me I'd be positive all right but they would have already
defined me as non-infected. To me that's a false-positive. Don't
you agree?

Dr : To be perfectly frank I think you are somewhat in denial over
this. Believe me I'm not having a go at you but that's what people
often do when the news is not good. You realise there are other tests
we could do to settle this matter?

P: You mean the viral load test?

Dr Yes.

P: But according to my packet inserts, when biotechnology companies and
the WHO investigate their tests, they don't do that. They don't go
checking the antibody positive people with viral load tests. So why do
it to me?

Dr: To reassure you?

P: There's a man I talked to this morning in the waiting room. He
told me he's had a positive antibody test since 1987. He didn't
have his first viral load test until 1992. In fact I know there were no
such things as viral load tests in 1987. And this man didn't have a
viral load test to prove his antibody test is correct. It was to do
with his drug treatment. If that man didn't need a viral load test
to diagnose him in 1987, why do I in 2004?

Dr : Because most of the people who come to this clinic have clearcut
reasons for being infected. Their cases are straight forward. I'm
sure from all your reading you wouldn't be surprised to know most of
our patients are either gay or drug users.

P: But doctor three weeks ago you told me I was infected with HIV.
You didn't say I was a difficult case. You didn't tell me I would
need another test to sort out my antibodies. And if I'd come to you
fifteen years ago with a positive test, before there were viral load
tests, surely you wouldn't have told me I wasn't infected.
That's not what happened to the man in the waiting room. And if it
wasn't for me and the Internet we wouldn't even be having this
conversation. And I understand what you are saying about gay men and
drug users. But to me that just makes the problem worse.

Dr : I'm beginning to think you must be reading some very unusual

P: All I've read is what's at PubMed. To find the paper on HIV in
the normal placenta I just entered "HIV p24 protein". Up it came.
Along with about 3000 others. So it took a bit of work. I assume
PubMed is where doctors do their literature searches. And the papers
there are peer reviewed?

Dr: Yes but why do you say the problem is worse in gay men and drug

P: Doctor I'm an actuary. I have a PhD in mathematics. From
Oxford. I came to Australia six years ago because my wife is a top
notch forensic scientist. She was head hunted by your National Crime
Commission. My field is statistics. I understand probabilities and
the like. That's what I'm paid to do. If you tell me a few things
about yourself I can tell what chance you have of getting any disease
you name and living to any age you care to say. If you want to know
the chance your wife will outlive you by a certain number of years I
can also tell you that.

Dr: I'm not questioning your competence in your field. But you seem
bent on questioning me in mine. Please tell me what problems do you
see with gay men and drug users.

P: You tell me any antibody molecule can cross-react. It can pick off
some protein it's not destined for. So let's assume that each
individual antibody molecule has some probability of a cross-reaction.
I have no idea what it is. Do you?

Dr: No. I don't think that kind of data is available.

P: OK but if healthy people with a normal number of antibodies have a
¼ probability of reacting with one of the ten HIV proteins the
probability can't be small. If a healthy person has say ten thousand
different antibodies, and a target of ten HIV proteins, you have a
hundred thousand combinations to try. That's a lot of locks and
keys. If you double the number of antibodies you have two hundred
thousand combinations. And that's just on numbers. I don't know
how variety affects the maths. So the more antibodies you have and the
more things you're exposed to and the more likely you will generate
an antibody that can cross-react in these tests. Or in any test for
that matter. And that's the problem. At least the way I see it.

Dr You'll have to explain.

P: Let's ask ourselves, what kind of people are likely to have the
greatest number and variety of antibody molecules? In general. Surely
the people in the AIDS risk groups must head the list? What about all
the germs and foreign substances that gay men and drug addicts are
exposed to? And haemophiliacs who get infused with foreign proteins
that come from thousands of blood donors. And what about Africans?
Who have all manner of diseases such as TB and fungal and parasitic
infections which also cause antibodies? And the organisms that cause
these diseases just happen to be representative of the commonest AIDS
defining diseases in Western AIDS patients. Who don't actually come
from Africa. So the groups of people with the greatest probability of
having cross-reacting antibodies, antibodies that will confuse these
tests, are the very groups in which you say the tests rarely make a
mistake. It just doesn't add up doctor. I'd say it would be a
miracle if any of the antibodies in AIDS patients were genuinely HIV.

Dr: I honestly don't follow your logic. You told me that the
laboratory test inserts your cousin sent from America confirmed the
antibody tests can separate patients with AIDS from patients who are
healthy. Isn't that right?

P: Yes there we agree. And we agree they do this very accurately.

Dr: Surely then if a positive antibody test distinguishes between AIDS
and healthy people then HIV must be involved in one group, the AIDS
patients, and not in the other group? The healthy people.

P: Why?

Dr: Because HIV causes AIDS. If the test distinguishes between AIDS
and not having AIDS then it automatically distinguishes between having
the cause of AIDS and not having the cause of AIDS. Which is HIV.
It's just another way of saying the same thing. It doesn't matter
which way around you say it.

P: No you can't deduce that doctor.

Dr : Why not? It can't be any other way. Unless of course you say
HIV is not the cause of AIDS. Surely you're not suggesting that?
Not seriously? Have you been reading some of the dissident junk on the

P: Have you read any of that junk doctor?

Dr: No of course not. Look, this is getting out of hand. There are
important things we must discuss and the sooner the better. We seem
stuck on what really shouldn't be a problem at all. I respect your
right to ask questions and I've tried my best to answer them but
obviously I'm not able to satisfy you. Perhaps you would prefer to
talk to one of my colleagues?

P: No that will not be necessary doctor. I have every confidence in
you. And in this clinic. Another doctor would only increase my
confusion. Let's call it a day. I'll try and come to come to
grips with it next time.

Dr: Very well. We certainly need to move on.

A week later.

P: Doctor I think I've worked out a way to explain my misgivings.

Dr: I'm glad to hear it.

P: Let's talk about tests in general terms. What actuaries do for
example. It's not too different from our last discussion.

Dr: OK.

P: Actuaries are interested in how long people live. Which is another
way of saying when people die. So we collect data about large groups
of people who have something in common. People who have say heart
disease or diabetes. We work out whether having or not having one of
these diseases will affect a person's chances of being or not being
alive at some future date. In a statistical sense of course.

Dr: Go on.

P: So what we do is very similar to your antibody tests and AIDS. Your
take people with or without a positive antibody test and contrast that
with the risk of having or getting AIDS or staying healthy.

Dr: Yes.

P: Now this is where I think the medical profession or the laboratory
scientists or whoever decides these things have gone beyond their data.
The outcome actuaries seek is whether a person is dead or alive. And
one of the 'tests' we use, is what diseases they have or don't
have at various times before they die. So our tests are diseases and
our outcome is death. Clear and unambiguous. You're either dead or
you're not.

Dr: Go on.

P: We don't use a substitute for dead bodies. We don't count the
numbers of death notices in the papers. We don't tally up how much
timber undertakers order. Or how small the forests are becoming. We
don't ask Centre Link how many pensions they've cancelled. We go
straight to the real thing.

Dr OK.

P: When it comes to the antibody tests the medical profession doesn't
deal with the real thing.

Dr: I don't follow.

P: You told me the antibody tests diagnose HIV infection.

Dr: That's right.

P: But you haven't produced any evidence for that. What you've
described is a test for AIDS. That's what you said you measure
antibodies against. The biotechnology companies and the WHO say it
too. You have a test for HIV but you measure it against AIDS.

Dr: I already explained that...

P: I know. You say you can use AIDS as a substitute for HIV. And not
having AIDS as a substitute for not having HIV. Well I don't think
you can do that.

Dr: Why not?

P: Several reasons. First: AIDS is not HIV. They're totally
different. AIDS is 30 diseases. HIV is allegedly a virus. Second:
The AIDS diseases have been around for hundreds, maybe thousands of
years. Long before we had AIDS. There's an account of Kaposis'
sarcoma in the Ebers papyrus. From ancient Egypt. Dating from 2500
BC. So if HIV is really a virus and does cause the AIDS diseases
it's not the only cause. It's not unique. How about tuberculosis?
TB has been found in Egyptian mummies. Would you use an Egyptian
mummy as a substitute for HIV?

Dr This is beginning to sound ridiculous...

P: You can use AIDS as an HIV substitute if and only if the sole cause
of these 30 diseases is HIV. Which it isn't. There's no way
around that. If you want to say AIDS can be substituted for HIV then
actuaries can substitute death for the number of cancelled pensions.

Dr Hold on...

P: The other faulty piece of logic is to use an antibody test as part
of the AIDS diagnosis. If a positive antibody test is part and parcel
of having AIDS it stands to reason there will be a perfect correlation
between these antibodies, wherever they come from whatever they are,
and AIDS. But that would be a man made correlation.

Dr: Look we may diagnose AIDS with an antibody test now but that was
not what we did when the HIV tests were developed. They were verified
against AIDS. A clinical diagnosis of AIDS. By that I mean history
and examination. Plus a few test like X-rays. But not antibody tests.
But when we did an antibody test, as an experiment if you like,
that's when we discovered all AIDS patients have these antibodies.
And if you don't have these antibodies you don't have AIDS. And
that has been found time after time. That's why an antibody test is
now part of the diagnosis.

P: Doctor that doesn't prove the antibodies are caused by HIV. It
just proves that AIDS patients have some antibodies which react with
these proteins in the test kits. Which you say could be cross-reacting
and therefore not HIV. So what you have is a blood test for AIDS. Or a
blood test that predicts an increased likelihood you will get sick from
certain diseases. That's fine if that's what you want. But
that's not the same thing as proving the antibodies are caused by a


P: There's more doctor. Third: A couple of weeks ago I suggested I
was a false positive. You didn't agree. That means you want to have
things both ways. If you're a biotechnology company you want to use
people like me as stand ins for being HIV free. You can read it in
their inserts. The one I have says 'Random donors are assumed to
have a zero prevalence of HIV antibody". So that's the rule.
Once you set up the rules you can't break them. Which means anyone
in this group who's positive must be recorded as a false positive.
But the same person sitting in your clinic the next day is truly
infected. That could easily apply to me.

Dr: I really think all your reading has made you quite confused.

P: What I understand doctor is this: If biotechnology companies and
the World Health Organisation are quite happy to use people without
AIDS including healthy people as HIV-free substitutes to verify their
tests then there can be no epidemic of HIV.

Dr: How on Earth do you come to that conclusion?

P: Because most people on Earth with a positive antibody test don't
have AIDS and in fact most are healthy.

Dr: You're telling me all those people, millions of them, 30% of some
African countries, aren't infected with HIV? They're all false

P: It's not me saying that doctor. I'm only drawing a conclusion
based on the rules you and the WHO recommend and approve. I don't
make up the rules. I'm just saying you should stick to them.

Dr: Is there anything else?

P: Have you ever read a packet insert?

Dr : No. I don't do the tests. They're done by the laboratory

P: Do they read the packet inserts?

Dr: I don't know.

P: Don't the agencies that approve the tests read them?

Dr: I don't know that either.

P: Can I read you something else from my packet insert?

Dr: Sure.

P: Both my packet inserts say "At present, there is no recognized
standard for establishing the presence or absence of antibodies to HIV
in human blood". What's your opinion on that statement doctor?

Dr: I'd like to hear your opinion.

P: OK. My opinion is that biotechnology companies employ a lot clever
people. And if a biotechnology company was developing a pregnancy test
someone in the organisation would know the recognised standard for
pregnancy is whether or not a woman has a baby. So it's not rocket
science to know that the recognised standard for a test to diagnose HIV
is whether or not the person has HIV. If that's what the test is for
that's what it should judged against. Which means the biotechnology
companies know these tests are not being judged against HIV itself.
Otherwise they wouldn't be saying what they do.

Dr: So you do not accept what I explained before?

P: Doctor I'm commenting on a packet insert. I'm offering my
opinion that the biotechnology companies must know HIV is the gold
standard method for validating the antibody tests but that it's not
being used. Why this is so I don't know. And why test manufacturers
repeatedly warn whoever reads their packet inserts about this I don't
know either. But I'm going to try and find out.

Dr: So what would actuaries have us do?

P: I can only speak for this actuary doctor. You've already told me
that cross-reacting antibodies can react in the HIV test. You said
that in the Western blot one or two antibodies are most likely caused
by cross-reactions and not HIV. When I asked how you know that you
said it's because of the band patterns the antibodies form. I
don't see how patterns or numbers distinguish between real and
cross-reacting antibodies. I don't believe you can know what
something is just because there's more of it. That's why I said
maybe all antibodies in these tests are cross-reacting and not HIV. Or
maybe they really are all HIV. Well there's an easy way to find out.

Dr: And what's that?

P: Use the virus. Do an experiment comparing the antibodies against
the virus itself. After all, that's what the test is for. It's a
test for HIV. It's not a test for AIDS.

Dr: And how would you do that?

P: Take say a thousand people. Some with AIDS, some with other
diseases like AIDS, some with diseases which are not AIDS and some
healthy people. You can't restrict your choice of non-AIDS people to
those who are healthy. If you do you'll be avoiding the problem of
cross-reacting antibodies. The non-AIDS group must include sick people
because these are the people who are likely to have generated increased
amounts of different antibodies that might confound the test. If you
only use healthy people you don't expose the test to enough
cross-reacting antibodies. Then you compare having or not having a
positive antibody test with having or not having HIV. As proven by
virus isolation. But, as the test manufacturers tell us in a round
about way, this has not been done. And it should have been done long
before the tests were used on the general population.

Dr: Well what are you going to do about your tests?

P: For the next three months I'm going to try and forget I have a
positive test. Actually I'm encouraged by something else I read in
the packet insert. "The risk of an asymptomatic person with a
repeatably reactive serum sample developing AIDS or an AIDS-related
condition is not known". So it seems no one is very sure what a
positive test means outside a risk group. Meantime I'll go to my GP
to make sure I haven't got TB or something else that might set these
tests off. I got immunised for 'flu and tetanus about three months
ago. Maybe that's the reason. I know I could be wrong so my wife
and I will put off having a baby and we'll use condoms. And I'm
going to spend a lot of my spare time in the library. Working out a
few things. Including why the HIV proteins occur in normal, healthy
people. In fact I'm going to read all the original papers on HIV
isolation and find out exactly what evidence international scientists
published to prove there is a virus called HIV. Then I'm going to
ask you to repeat my test.

Dr: And what if your test is still positive?

P: Then whatever caused it must still be operative. But that won't
prove it's HIV.


Next question


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Monoclonal antibodies to the human immunodeficiency virus p18 protein
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Posts: 93

PostPosted: Sat Jul 15, 2006 9:02 am    Post subject: Re: AIDS Reply with quote

In the third paragraph of my post above, "someone" should be "somehow."
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Joined: 07 May 2005
Posts: 193

PostPosted: Sat Jul 15, 2006 12:02 pm    Post subject: Re: AIDS Reply with quote

On 15 Jul 2006 02:00:19 -0700, monty1945@lycos.com wrote:

This is "old news," TC. I'd suggest people read posts at
http://groups.msn.com/aidsmythexposed/general.msnw or read some of the
essays at www.theperthgroup.com for more up to date information.

Except none of that is up-to-date. The Perthies have never done an
experiment in their lives--and their claim that HIV doesn't exist is
ridiculous. If that were the case, NO infectious agent would exist
because the exact same techniques they decry are used to isolate many
of them.

There is a very good discussion on BMJ that actually provides a good
back-and-forth on the deeper technical details if anyone is

George M. Carter
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Joined: 07 May 2005
Posts: 193

PostPosted: Sat Jul 15, 2006 12:13 pm    Post subject: Re: AIDS Reply with quote

On 15 Jul 2006 02:00:19 -0700, monty1945@lycos.com wrote:

Otherwise, if the virus was doing something nasty for all those years,
it would have been detected already, over 20 years since the Gallo
press conference.

Ah...it has been--by a whole slew of scientists.

There are also misleading statements in this entry quoted by Mr.
Carter. I don't have the time to speak on every one, but let us take
the following simple one:

"HIV belongs to a subgroup of retroviruses..."

However, retroviruses are of a certain size and shape, and despite
numerous attempts to do so, nothing of the right size and shape has
been found in any tissue of anyone said to be infected with "HIV" or
dying of "AIDS,"

Well, no, this is again an error. For example, there are a lot of
people looking at the genetic history of HIV species. For example:


The Perthies, who do NOT do experiments are about the ONLY people who
think HIV doesn't exist. Everyone else who IS doing experiments has no
trouble finding it. Even Duesberg realize it exists.

But then I expect little more from you than you'd embrace the most
outre and pointless argument of the whole ridiculous lot.

I guess what saddens me is that this nonsense has some really horrible

1) Some people might choose to believe it--like David Pasquarelli did.
They then become HIV-infected, wind up with AIDS and die. Like he did.

2) It deflects from the quite serious and horrific political problems
that HIV/AIDS exposes--
a) stigma and discrimination against the ill;
b) stigma and discrimination against vulnerable populations
(males who have sex with males, injection drug users, prisoners, sex
c) the failure of the government to institute effective
prevention programs and--in the US--the embrace of the scientifically
invalid approach of "abstinence only";
d) the hubris of the Pentagon and others for following the
subunit env vaccine down the road to perdition--putting many lives at
risk for an obvious failure candidate vaccine;
e) the crimes against humanity committed by the US Government
and the pharmaceutical industry in denying people access to treatment
on the mistaken beliefs that (i) intellectual property rights trump
human life and (ii) intellectual property rights equate with
profiteering and enriching CEOs and stockholders (instead of

I wonder if Tom will really get himself infected. I hope not. As not
only would it be tragically stupid, but, like David Pasquarelli, his
eventual death from AIDS will be ignored by the denialists that
survive him.

George M. Carter
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medicine forum addict

Joined: 02 Apr 2006
Posts: 93

PostPosted: Sat Jul 15, 2006 3:15 pm    Post subject: Re: AIDS Reply with quote

I agreee with Mr. Carter about the BMJ debate. Take a look at it and
decide for yourself. One link is:

The problem with saying that the Perth Group has not done an experiment
is that they seek funding but only those who agree with the "HIV/AIDS"
claim can get that amount of funding. However, this does not preclude
them from using human reason to point out that if you never find the
virus, but only "markers" that can be generated by totally non-viral
phenomena, then your "theory" is in big trouble. Notice that Mr.
Carter does not provide a citation for an experiment that detected
particles of the correct size and shape in those said to be HIV
infected or dying of AIDS. This is the kind of evidence that would be
necessary in order to begin to formulate a hypothesis that might blame
a virus. Moreover, if you look at the literature written by the "virus
huinters" themselves, they point to the inflammatory response and the
dangerous element, and that would take hours or days, not more than a
decade, to happen. I have numerous quotations from these virus hunters
on my web site essays, for those interested.

However, due to the way "HIV/AIDS" is defined (in a way antithetical to
the scientific method) and also the fact that people who "test
positive" most likely are leading very unhealthy lives (and let's not
forget how many "AIDS patients" die of livers damaged by the
"medicines" today), it's no surprise that one can say something like,
"look at all the people dying of AIDS who tested positive many years
ago." I'm surprised the numbers are not higher, actually. Supposedly,
this terrible infectious pandemic "HIV/AIDS" kills hardly any female
prostitutes in the USA who don't do IV drugs, and in fact only
supposedly kills about 14,000 a year in the USA these days - not on the
top of the list by any means. Hospital infections, which are
completely avoidable, kill 90,000 or so each year. Avoidable accidents
at work kill around 40,000 or so, and just think about how many are
killed in automobile accidents. "HIV/AIDS" has become a big business,
and those who tell you that you need to fear a "retrovirus" 12 years
later are mostly totally conflicted, making money and/or holding
positions of power in the "industry" that "HIV/AIDS" has become.
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medicine forum Guru Wannabe

Joined: 07 May 2005
Posts: 193

PostPosted: Sat Jul 15, 2006 4:36 pm    Post subject: Re: AIDS Reply with quote

On 15 Jul 2006 08:15:55 -0700, monty1945@lycos.com wrote:

I agreee with Mr. Carter about the BMJ debate. Take a look at it and
decide for yourself. One link is:

LOL...right. A one-sided view of the debate. Why not try the original
source. That is

There is plenty of back-and-forth with the Perth group, which also
further underscores that denialist nonsense has NOT been silenced.
They've had the opportunity to air the tawdry laundry of their tiny
minds and been left flailing.

Sigh. It pisses me off, obviously--as it does you, I'm sure. But for
me it is personal. I do not want to see more people infected. I do not
want to lose more of my friends to AIDS. I've known hundreds of people
who have died of AIDS--very many dear and close friends. A tiny
fraction of the millions who have died.

For this stupid fucking debate to carry on like this in 2006 is simply
obscene. It is ridiculous and again, it deflects from the seriously
fucked up problems our world faces while you womble off into your
psychotic fantasy la-la land.

The problem with saying that the Perth Group has not done an experiment
is that they seek funding but only those who agree with the "HIV/AIDS"
claim can get that amount of funding.

Oh, horseshit. They wrote in Nature Biotechnology. They simply do not
have the ABILITY to do that kind of research.

However, this does not preclude
them from using human reason to point out that if you never find the
virus, but only "markers" that can be generated by totally non-viral
phenomena, then your "theory" is in big trouble.

This statement is gobbledy-gook. It means nothing. The reference I
provided above gives AMPLE resources.

HIV has been isolated. It is found in people with HIV infeciton and
AIDS. It is not found in people who do lots of recreational drugs, for
example, but do not have or develop AIDS.

Notice that Mr.
Carter does not provide a citation for an experiment that detected
particles of the correct size and shape in those said to be HIV
infected or dying of AIDS.

Are you claiming that such does not exist?

This is a patently false claim. See, for example,

Of course, if you wish to rely on criteria that are impossible to
meet, then of course you will be satisfied with your conclusion. This
is what the Perth Group does. Brian Foley notes: " The criteria that
the Perth group claim are needed are impossible to meet. No virus has
ever met them and none ever will. Density gradient ultracentifugation
can only "enrich" a virus preparation up to 80% to maybe 98% purity,
it can never produce a 100% "pure" virus preparation free of all other
materials. Several groups have made such preparations of HIV (as they
have for FIV, SIV, EIAV and other lentiviruses) and shown that there
is some cellular debris and microvessicles derived from the cell
culture in these preparations. Even 100% virus particles will contain
some cell-derived proteins, because lentiviruses are enveloped viruses
and the lipid bilayer envelope carries with it some cellular proteins
such as MHC molecules.

"Infectious molecular clones on the other hand can be made 100% pure,
free of even viral proteins, they are just naked DNA copies of the
viral genome. There are thousands of other advantages of cloning, over
crude density preps of viruses. Molecular genetics offers a whole
world of research that was not available with pre-1970 techniques."

In short, by Perth's standards, NO viruses exist. It's ridiculous--and
underscores why they are intellectually bankrupt.

I really have to laugh that Perth, in its vapid embrace of only ONE
method of sucrose-gradient density centrifugation that is acceptable
methodology in their little pea-brained minds, they cite Sinoussi F,
Mendiola L, Chermann JC, Jasmin C, Raynaud M. (1973) Purification and
Partial Differentiation of the Particles of Murine Sarcoma Virus (M.
MSV) According to their Sedimentation Rates in Sucrose Density
Gradients. Spectra 4:237-243.

Do you know who the first author is?

One guess.

The woman that discovered LAV, later known as HIV-1.

You'd think she might know a wee bit about viral isolation, wouldn't

This is the kind of evidence that would be
necessary in order to begin to formulate a hypothesis that might blame
a virus.

Bullshit. There are more data that you will willfully ignore as that
is the tautology of denialism that you suffer from:
amie Mills asks:
"Did either Bess et al. or Gluschankof et al. approach 80% or even 98%
purified virus, or what looks like purified virus?"

And the answer is YES. In the Bess paper, the HIV-1 isolate MN, clone
4 virus grown of CEM-SS cells produced a preparation that was more
than 99% pure. They discuss why there are differences in purity
depending on which cell line and which virus is used.

Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ.
Cell membrane vesicles are a major contaminant of gradient-enriched
human immunodeficiency virus type-1 preparations.
Virology. 1997 Mar 31;230(1):125-33.
PMID: 9126268

Bess JW Jr, Gorelick RJ, Bosche WJ, Henderson LE, Arthur LO.
Microvesicles are a source of contaminating cellular proteins found in
purified HIV-1 preparations.
Virology. 1997 Mar 31;230(1):134-44.
PMID: 9126269

"...how is that proof of an exogenous and infective retrovirus?"

No single experiment is "proof" of anything, really. There are whole
textbooks written about virology and retroviruses. I can't spell it
all out here. Endogenous retorviruses do exist, they are found in the
genomes of nearly all eukaryotes. If the virus in not found in the
germ-line DNA of an organism, it is not defined as endogenous, it is
exogenous. No complex retrovirus (such as the lentiviruses and the
T-cell leukemia viruses) which carry regulatory genes (tat, rev, nef,
vif, vpu, vpx etc) in addition to the gag pol and env retroviral
genes, have ever been found in an endogenous state in any host. A few
endogenous viruses have one or two potenital open reading frames in
addition to gag, pol and env, but none are truly complex. The closest
relative to lentiviruses found in the human genome are endogenous
retroviruses such as HERV-K, and these retroviral elements are very
clearly not HIV-1 or any other lentivirus.
As for infectious, the global pandemic of infections with many
different subtypes and circulating recombinant forms derived from the
HIV-1 M group of viruses pretty much answers that question. Whether
one studies infectious molecular clones of HIV-1, or transmission
chains such as the case of Nushawn Williams who infected 13 young
women, or local or country-wide epidemics, the answer is always

"... our local laboratories use proteins isolated from sucrose
gradients,(as mentioned in accompanying leaflets), ..."

How were those proteins grown before the sucrose gradient prpearation?
Was it clone whole virus grown on human cells? Or was it just viral
genes grown in E. coli? Do you observe a large false-positive rate
with the tests you are using? Just because sucrose gradients of HIV-1
whole virus particles are contaminated with varrying levels of
cellular vessicles when the virus is grown on human cell lines, does
not mean that all sucrose gradients are useless for all purposes.

"...If we then move on to western blots as a means of confirming a
diagnosis, how many bands and which do you need to confirm a
diagnosis? This varies considerably around the world and means a
person may be HIV positive in Africa but hop on a plane and have the
same test in Australia and be HIV negative! What does that mean for
our patients? ..."

No test of tests for any infection or any other medical condition
(such as pregnancy for an example) is always 100% perfect. What this
means for any patient, is that some human intelligence is required in
interpretting results. There are dozens of possible logical reasons
for either a false negative (very recent infection is the major one)
or false positive (the patient has elevated levels of some antibody or
antibodies that bind to HIV proteins) HIV ELISA test. This is why a
single ELISA is not the recommended standard for diagnosis. A person
truly cannot be HIV positive in one country and HIV negative in
another. They can be "officially" diagnosed as such, but they are
either infected or not regardless of that diagnosis. If a gets a
positive pregnancy test result with one test and negative with
another, it doesn't mean she is "partially pregnant", and the same
principles hold true for diagnosing HIV infection or any other
infection. More than 99% of people who are infected with HIV-1 develop
antibodies to many different HIV-1 proteins over time, such that some
bands on the western blot typically appear first, followed by others.
Also, very late in AIDS progression antibodies to some ands on the
western blot are prone to decline. The end result is that we should
expect a temporal variance in the number of reactive bands within any
one infected individual. It should also be noted that "reactivity" to
a protein band on a western blot is not a binary condition (wither
"yes" or "no") but an analog condition varying from weak to strong.

The end result is that both patients and doctors need to use other
data besides the ELISA and WB tests and human intelligence to
interpret that data. If a person has never had sex, never had a
transfusion, never injected drugs and has a weakly positive ELISA and
two weakly positive western blot bands, the sensible thing to do is to
wait a few months and re-test to see if this was just a spurious
problem. If the results are identical months later, then it might be
worth finding out what is causing them (perhaps infection with HTLV,
which is one of the closest relatives of the lentiviruses). On the
other hand if reactivity has increased to a strong ELISA positive plus
3 or 4 strongly reactive western blot bands, there is little (but
still some) doubt that the person is truly infected, and further tests
should be done to find out for sure, and if so, to find out how this
person could have become infected (perhaps they were not fully honest
about sex, or IV drug use, or perhaps they will be the clue that
uncovers a new route of transmission as Kimberly Bergalis was in the
famous "Florida Dentist" case).

Moreover, if you look at the literature written by the "virus
huinters" themselves, they point to the inflammatory response and the
dangerous element, and that would take hours or days, not more than a
decade, to happen. I have numerous quotations from these virus hunters
on my web site essays, for those interested.

LOL...more nonsense. Chronic inflammatory responses cause disease in a
variety of settings from Hepatitis B or C chronic infections to
rheumatoid arthritis.

However, due to the way "HIV/AIDS" is defined (in a way antithetical to
the scientific method) and also the fact that people who "test
positive" most likely are leading very unhealthy lives (and let's not
forget how many "AIDS patients" die of livers damaged by the
"medicines" today), it's no surprise that one can say something like,
"look at all the people dying of AIDS who tested positive many years
ago." I'm surprised the numbers are not higher, actually.

That's the point. If "lifestyle" caused AIDS, there would be a HELL Of
a lot of dead straight people in the US who died from infections like
pneumocystis. And a lot of LIVING people--many whom I have personally
known--men, women, children, straight, gay, whatever -- who did NOT
have a particularly hardcore lifestyle. They DID have HIV and too many
of my friends have died of AIDS.

Your ongoing dithering bullshit is a distraction from the fight
against AIDS--and the political nightmare that arises in terms of
healthcare access that affects EVERYONE in the US--including 47
million of us lacking insurance, as an example.

this terrible infectious pandemic "HIV/AIDS" kills hardly any female
prostitutes in the USA who don't do IV drugs, and in fact only
supposedly kills about 14,000 a year in the USA these days - not on the
top of the list by any means.

More unsupported, declarative statements. Back this nonsense up.

Hospital infections, which are
completely avoidable, kill 90,000 or so each year. Avoidable accidents
at work kill around 40,000 or so, and just think about how many are
killed in automobile accidents. "HIV/AIDS" has become a big business,
and those who tell you that you need to fear a "retrovirus" 12 years
later are mostly totally conflicted, making money and/or holding
positions of power in the "industry" that "HIV/AIDS" has become.

LOL. I'm not and most of the people I know in the fight against
HIV/AIDS are not. That's just a pathetic dodge in the first part to
say other things kill people (duh) and an attack the messenger lie on
the second part that puts you on a par with Karl Rove.

More abstracts below.

George M. Carter

Regier DA, Desrosiers RC.
The complete nucleotide sequence of a pathogenic molecular
clone of simian immunodeficiency virus.
AIDS Res Hum Retroviruses. 1990 Nov;6(11):1221-31.
PMID: 2078405

Takeuchi H, Suzuki Y, Tatsumi M, Hoshino H, Daar ES,
Koyanagi Y.
Isolation and characterization of an infectious HIV type 1
molecular clone from a patient with primary infection.
AIDS Res Hum Retroviruses. 2002 Oct 10;18(15):1127-33.
PMID: 12402946

Mochizuki N, Otsuka N, Matsuo K, Shiino T, Kojima A, Kurata
T, Sakai K, Yamamoto N, Isomura S, Dhole TN, Takebe Y,
Matsuda M, Tatsumi M.
An infectious DNA clone of HIV type 1 subtype C.
AIDS Res Hum Retroviruses. 1999 Sep 20;15(14):1321-4.
PMID: 10505681

Novelli P, Vella C, Oxford J, Daniels RS.
Construction and characterization of a full-length HIV-1(92UG001)
subtype D infectious molecular clone.
AIDS Res Hum Retroviruses. 2002 Jan 1;18(1):85-8.
PMID: 11804560

Ndung'u T, Renjifo B, Novitsky VA, McLane MF, Gaolekwe S,
Essex M.
Molecular cloning and biological characterization of
full-length HIV-1 subtype C from Botswana.
Virology. 2000 Dec 20;278(2):390-9.
PMID: 11118362

Ndung'u T, Renjifo B, Essex M.
Construction and analysis of an infectious human
Immunodeficiency virus type 1 subtype C molecular clone.
J Virol. 2001 Jun;75(11):4964-72.
PMID: 11333875

Takahoko M, Tobiume M, Ishikawa K, Ampofo W, Yamamoto N,
Matsuda M, Tatsumi M.
Infectious DNA clone of HIV type 1 A/G recombinant
(CRF02_AG) replicable in peripheral blood mononuclear cells.
AIDS Res Hum Retroviruses. 2001 Jul 20;17(11):1083-7.
PMID: 11485626

Earlier papers:

Adachi A, Ono N, Sakai H, Ogawa K, Shibata R, Kiyomasu T,
Masuike H, Ueda S.
Generation and characterization of the human
immunodeficiency virus type 1 mutants.
Arch Virol. 1991;117(1-2):45-58.
PMID: 1706590

Kuwata T, Igarashi T, Ido E, Jin M, Mizuno A, Chen J,
Hayami M.
Construction of human immunodeficiency virus 1/simian
immunodeficiency virus strain mac chimeric viruses
having vpr and/or nef of different parental origins and their in vitro
and in vivo replication.
J Gen Virol. 1995 Sep;76 ( Pt 9):2181-91.
PMID: 7561755

Collman R, Balliet JW, Gregory SA, Friedman H, Kolson DL,
Nathanson N, Srinivasan A.
An infectious molecular clone of an unusual
macrophage-tropic and highly cytopathic strain of human
immunodeficiency virus type 1.
J Virol. 1992 Dec;66(12):7517-21.
PMID: 1433527

Dirckx L, Lindemann D, Ette R, Manzoni C, Moritz D, Mous J.
Mutation of conserved N-glycosylation sites around the
CD4-binding site of human immunodeficiency virus type 1
GP120 affects viral infectivity.
Virus Res. 1990 Dec;18(1):9-20.
PMID: 2082620

Fisher AG, Collalti E, Ratner L, Gallo RC, Wong-Staal F.
A molecular clone of HTLV-III with biological activity.
Nature. 1985 Jul 18-24;316(6025):262-5.
PMID: 2410792

Popovic M, Sarngadharan MG, Read E, Gallo RC.
Detection, isolation, and continuous production of
cytopathic retroviruses (HTLV-III) from patients
with AIDS and pre-AIDS.
Science. 1984 May 4;224(4648):497-500.
PMID: 6200935

Ghrayeb J, Kato I, McKinney S, Huang JJ, Chanda PK,
Ho DD, Sarangadharan MG, Chang TW, Chang NT.
Human T-cell lymphotropic virus type III (HTLV-III)
core antigens: synthesis in Escherichia coli and
immunoreactivity with human sera.
DNA. 1986 Apr;5(2):93-9.
PMID: 3011373

Heidecker G, Lerche NW, Lowenstine LJ, Lackner AA, Osborn
KG, Gardner MB, Marx PA.
Induction of simian acquired immune deficiency syndrome
(SAIDS) with a molecular clone of a type D SAIDS retrovirus.
J Virol. 1987 Oct;61(10):3066-71.
PMID: 3041028

Fisher AG, Ratner L, Mitsuya H, Marselle LM, Harper ME,
Broder S, Gallo RC, Wong-Staal F.
Infectious mutants of HTLV-III with changes in the 3'
region and markedly reduced cytopathic effects.
Science. 1986 Aug 8;233(4764):655-9.
PMID: 3014663

Adachi A, Gendelman HE, Koenig S, Folks T, Willey R,
Rabson A, Martin MA.
Production of acquired immunodeficiency syndrome-associated
retrovirus in human and nonhuman cells transfected
with an infectious molecular clone.
J Virol. 1986 Aug;59(2):284-91.
PMID: 3016298

Sakai K, Dewhurst S, Ma XY, Volsky DJ.
Differences in cytopathogenicity and host cell range
among infectious molecular clones of human
immunodeficiency virus type 1 simultaneously
isolated from an individual.
J Virol. 1988 Nov;62(11):4078-85.
PMID: 3172338

Sakai K, Ma XY, Volsky DJ.
Low-cytopathic infectious clone of human immunodeficiency
virus type I (HIV-I).
FEBS Lett. 1988 Oct 10;238(2):257-61.
PMID: 2458968

More papers related to serological analysis of the products
of cloned HIV genes, etc.

Chandra A, Gerber T, Kaul S, Wolf C, Demirhan I, Chandra P.
Serological relationship between reverse transcriptases from
human T-cell lymphotropic viruses defined by monoclonal
antibodies. Evidence for two forms of reverse
transcriptases in the AIDS-associated virus, HTLV-III/LAV.
FEBS Lett. 1986 May 12;200(2):327-32.
PMID: 2423366

Chakrabarti LA, Ivanovic T, Cheng-Mayer C.
Properties of the surface envelope glycoprotein associated
with virulence of simian-human immunodeficiency virus
SHIV(SF33A) molecular clones.
J Virol. 2002 Feb;76(4):1588-99.
PMID: 11799153

Gorny MK, Williams C, Volsky B, Revesz K, Cohen S, Polonis
VR, Honnen WJ, Kayman SC, Krachmarov C, Pinter A,
Zolla-Pazner S.
Human monoclonal antibodies specific for conformation-
sensitive epitopes of V3 neutralize human
immunodeficiency virus type 1 primary isolates from
various clades.
J Virol. 2002 Sep;76(1Cool:9035-45.
PMID: 12186887

Zhang PF, Bouma P, Park EJ, Margolick JB, Robinson JE,
Zolla-Pazner S, Flora MN, Quinnan GV Jr.
A variable region 3 (V3) mutation determines a global
neutralization phenotype and CD4-independent infectivity
of a human immunodeficiency virus type 1 envelope
associated with a broadly cross-reactive, primary virus-
neutralizing antibody response. J Virol. 2002 Jan;76(2):644-55.
PMID: 11752155

Ball JM, Payne SL, Issel CJ, Montelaro RC.
EIAV genomic organization: further characterization by
sequencing of purified glycoproteins and cDNA.
Virology. 1988 Aug;165(2):601-5.
PMID: 2841805

Rekosh D, Nygren A, Flodby P, Hammarskjold ML,
Wigzell H.
Coexpression of human immunodeficiency virus envelope
proteins and tat from a single simian virus 40 late
replacement vector.
Proc Natl Acad Sci U S A. 1988 Jan;85(2):334-8.
PMID: 2829181
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Will Brink
medicine forum addict

Joined: 11 Mar 2005
Posts: 83

PostPosted: Thu Jul 20, 2006 10:15 pm    Post subject: Re: AIDS Reply with quote

In article <1152912057.518304.111590@p79g2000cwp.googlegroups.com>,
"TC" <tunderbar@hotmail.com> wrote:


Science by press conference
Gallo's original Science papers, a relevant section of which is
reproduced here, claimed "isolation" of HIV only in 30.2% of adult AIDS
cases with Kaposi's sarcoma, and 47.6% of adult AIDS cases with
opportunistic infection. This is the evidence based on which Gallo,
with the blessings of Reagan's Secretary of Health and Human Services,
Margaret Heckler, told the world press on April 23th, 1984 (two weeks
before publication of the Science papers), that he had found the
"probable cause of AIDS"!

You mean after he stole it from the French?

Will Brink @ www.BrinkZone.com
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Will Brink
medicine forum addict

Joined: 11 Mar 2005
Posts: 83

PostPosted: Thu Jul 20, 2006 10:16 pm    Post subject: Re: AIDS Reply with quote

In article <1152912057.518304.111590@p79g2000cwp.googlegroups.com>,
"TC" <tunderbar@hotmail.com> wrote:


It was later revealed that Gallo had stolen his samples from French
researcher Luc Montagnier.

My bad. Didn't see this part.

Will Brink @ www.BrinkZone.com
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