article on viral load

interesting HIV & AIDS - Viral Load and the PCRVIRUSMYTH HOMEPAGE




VIRAL LOAD AND THE PCR
Why they can't be used to prove HIV infection
By Christine Johnson
Continuum Nov. 2001

"Biotechnology's version of the Xerox machine" -- that's what Forbes
magazine called the polymerase chain reaction (PCR). This revolutionary
technique enables a scientist to take a sample containing a minute
amount of DNA and replicate that DNA sequence until there are a million
copies instead of just one or two.
Kary Mullis, inventor of PCR, won a 1993 Nobel prize for his
billion-dollar invention, which has become indispensable to any genetics
lab. It is ironic that one of the first applications of PCR was to
detect HIV, considering that Mullis himself doesn't believe his
invention is capable of this. Mullis states the problem is PCR is too
efficient -- it will amplify whatever DNA is in the sample, regardless
of whether that DNA belongs to HIV or a contaminant. And how do you
decide which part of the amplified material could be HIV and which part
the contaminant(s), if you couldn't detect HIV in the sample without
using PCR?
One of the main arguments against the HIV/AIDS hypothesis is that, when
employing traditional methods of virus detection, HIV has never been
inferred in significant amounts in people with AIDS. Virus culture, for
instance, has been adequate to find other viruses, but not HIV. Why not?
When virus culture is employed to detect HIV, HIV is never seen or even
looked for in the cultures. Its presence is measured by very indirect
methods: assays for detection of reverse transcriptase or a p24 protein,
neither of which is specific for HIV. Indirect methods would not be
necessary if a significant amount of HIV were there to begin with.
In other words, if a meaningful amount of HIV were present, the
time-honoured laboratory techniques should be able to find it. They
can't. Now we need not only PCR, but continuous modifications and
improvements on PCR, in order to try to find HIV.
This is how the idea of "viral load" came about, inspired by two spates
of scientific papers that claimed HIV is busily replicating by the
billions: initially, papers claiming HIV was "hiding in the lymph
nodes," (1,2) and more recently, the Ho and Wei papers. (3,4) The latter
studies attempted to measure "viral load" at a given point, after which
"antiviral" drugs were administered to the patient. The drugs were
supposed to prevent replication of any new HIV, and the viral load would
decrease accordingly. However, within a few days, the remaining virus
would mutate into a form resistant to the drugs, and in a few weeks the
viral load would return to its pre-treatment levels. Applying a
mathematical formula to this dynamic, the rate at which the virus
replicates was allegedly determined.
Hence was born what I call "Dr. Ho's kitchen sink theory". According to
Ho, billions of copies of HIV are being made every day, which infect
billions of T4-cells. These T-cells are destroyed not by HIV, but by the
immune system. They are replenished every day, but over the years, the
immune system loses ground and HIV finally wins. This process was
likened to a sink with the drain open, the water pouring in from a tap
(new T-cells being made) at a slightly lower rate than it drained away
(infected T-cells being destroyed).
It is most important to note that the viral load studies all rely
completely on PCR and related techniques. This article will discredit
PCR as an accurate method of determining HIV infection, which will in
turn cast doubt on any conclusions about HIV that have been made based
on PCR techniques.
Some Basics On DNA
PCR takes advantage of certain fundamental properties of DNA. DNA (as
well as RNA) is a nucleic acid, and nucleic acids are composed of
nucleotide "building blocks". DNA exists as two complementary strands
arranged in a double helix formation (two intertwining spirals). These
strands are made up of many nucleotides hooked together to form a long
chain of DNA.
The nucleotide molecule has three different parts: the phosphate and the
sugar (which form a backbone or a ribbon-like structure), and the base.
There are four types of bases: A, T, C, and G (adenine, thymine,
cytosine, and guanine). These bases are attached to the backbone, which
is wound in the familiar double helix.
The bases on one strand bind to the bases on the other strand, and this
gives DNA its stable double helix structure. (Think of the two strands
as forming a zipped-up zipper.) The distinct nature of an organism's DNA
code depends on the order, or sequence, of the bases along the DNA
chain.
There are special rules about how bases form chemical bonds with other
bases: an A will only bind to a T, and a C will only bind to a G. A base
on one strand binding to a base on the other strand is called a
"complementary base pair". This rule of complementary base pairing is
what gives DNA its ability to replicate itself exactly.
Each time a cell divides, it has to make a copy of its DNA for the new
cell. The DNA double-strand first "unzips" itself into two separate
strands. Each single strand serves as a template, or pattern, from which
to make a new copy of its complementary strand. (So, strand #1 serves as
a pattern to make a new copy of strand #2, and vice versa.) The single
strand then incorporates new nucleotide building blocks from the
surrounding medium according to the rule of complementary base pairing.
In other words, an available A on the single strand will grab onto a T
nucleotide, a C will grab a G, and so on until the entire opposite
strand is duplicated. At the end of this process, the two original
strands zip themselves up again, and the two copied strands serve as DNA
for a new cell.
How PCR Works
The theory of HIV says it, like other suggested retroviruses, contains
RNA but no DNA: when HIV is said to infect a cell, the reverse
transcriptase enzyme is thought to transform the RNA into complementary
DNA, which is then inserted into the host cell's DNA.
Therefore, if PCR is used to analyse human tissue for the presence of
HIV, it would be looking for only a short segment out of the entire
cellular DNA strand. This short segment represents the genetic material
proposed for HIV, that in theory has been incorporated into the DNA of
the cell. (Viral load studies try to look for cell-free HIV. Even here,
PCR is only looking for part of HlV's entire proposed genetic package,
or genome, not an entire virus.)
PCR works in the following fashion:
Step 1: Heat the template. A long piece of DNA containing the smaller
fragment to be copied is heated. The two strands can be "melted" apart
at elevated temperatures, and will slowly come back together upon
cooling ("annealing"). The two separated strands are complementary to
each other. They serve as templates for the new strands.
Step 2: Add the primers. Something called a primer is necessary for the
next step. Primers are nucleotides that form a short sequence of new
strand. Primers are designed to be complementary to a known sequence
which is part of a larger sequence, and thus where the primers will bind
(or hybridise) is known.
The primers attach to each end of the DNA segment that is to be copied
(the segment that represents HIV's proposed genetic material). The
primers serve two purposes: a) to mark each end of the targeted segment
so only that segment will be amplified, and not the entire strand, and
b) to get the duplication process started. The new strands are built
block by block by the action of an enzyme called polymerase. The
polymerase builds a new DNA strand alongside an existing strand. The
polymerase will not work unless the old strand (the template) already
has on it a few nucleotides forming a short sequence of new strand (the
primer). (If you ever see a reference to "template-primers," this is
what they're talking about.)
In other words, the polymerase can only form a new strand if the new
strand has already partially been formed. In nature, when your own DNA
is duplicating itself, other enzymes called DNA primases build the
primer onto the old strand.
Once the polymerase gets going, it crawls along the single DNA strand
(the template) adding to it the nucleotide building blocks one by one.
The primer ends up being part of the newly-made strand.
In nature, polymerases pull the DNA strands apart while they build the
new DNA strand. This is how duplicate copies of DNA are made so that
cells like blood and skin cells can divide into two new cells, a process
essential for life.
Step 3: Amplify. Once again, after melting and then annealing the
primers, the polymerase enzyme copies the DNA beginning at the primer,
making a new copy of each target segment. This process is repeated for
as many as 30-40 rounds. During each cycle, the amount of segments
doubles, so two segments become four, four become eight, then 16, etc.
By the end of the process, approximately a million copies of the
original segment have been made. Now you have a whole lot of DNA, where
originally you had only a minuscule amount. This is why PCR is referred
to as being able to find a "needle in a haystack."
Obviously, it is necessary for the primers to be specific to HIV.
Whether the PCR will make an amplified product (a "positive PCR")
depends on whether the primers you add match part of the DNA in the
target specimen.
Below, we will see that the specificity of the primers for HIV is in
doubt. Even if the primers were specific to HIV, if similar sequences
are present in the target, the primers, under lax conditions, will form
hybrids with (or bind) related sequences that are less than a perfect
match. They will then prime the polymerase, which starts the
amplification procedure, even though no HIV was present to begin with.
Using PCR To Find HIV
A problem for the HIV hypothesis was that, even with the use of standard
PCR, researchers could not find much, if any, HIV in persons with AIDS
diagnoses. To resolve this paradox, the authors of the new "viral load"
papers came up with two modifications of PCR, which they claimed were
much more efficient at finding HIV. These were the QC-PCR and the
branched DNA test (bDNA). And suddenly -- eureka! -- billions of copies
of what was believed to be HIV were found. The contradiction here seems
to have escaped the authors of these papers: Why would such powerful new
tests be needed at all to find a microbe that is present in the
billions? Traditional methods should suffice.
QC-PCR
This is the test used in the above-mentioned papers by Anthony Fauci
(Pantaleo) and Ashley Haase (Embretson), which claimed HIV was "hiding
in the Iymph nodes." These papers were accepted as fact, even though
QC-PCR was, and remains, an unvalidated technique.
Mark Craddock, of the University of Sydney (Australia), explained the
principles of and problems with QC-PCR as follows: (8)
"PCR mass produces fragments of DNA. You start with a small amount of
DNA and after each PCR cycle, the amount of DNA you have is between one
and two times the amount at the beginning of the cycle. Thus, the amount
of DNA you have to study increases exponentially. The fact that the PCR
is an exponential growth process means that experimental errors will
also grow exponentially, so you need to be very careful about what you
do with the process.
"A number of people have decided that it should be possible to estimate
the amount of DNA present in a sample by using PCR. This is the
so-called quantitative competitive PCR. The idea is to add to the sample
to be estimated a known amount of similar but distinguishable DNA and
amplify both together. The assumption is that the relative amounts of
the two products should stay the same, and hence you can work out the
size of the sample you started with by knowing the ratio of the two,
determined by observation when PCR has produced enough of both to
measure, and how much control DNA was added.
"What is absolutely crucial is that the relative amounts of the test DNA
and your known control must remain exactly equal. Close is not good
enough. The slightest variations will be magnified exponentially and can
produce massive errors in your estimate.
"The difficulties in using PCR quantitatively were pointed out by Luc
Raeymaekers in the journal Analytical Biochemistry in 1993. He noted
published papers on QC-PCR contain data that show that the fundamental
assumption that the relative sizes of the samples remain constant is not
met in practice. Despite this, HIV researchers continue to use PCR to
quantify viral load. There is simply no way of knowing whether a given
estimate is correct or is 100,000 times too high!"
Todd Miller calls QC-PCR the "latest fad in science" and agrees that if
the relative amounts of your test DNA and your known control are not
equal, there is one thing you can say for sure about the estimate of
your starting target (the amount of proposed HIV RNA in the patient's
blood sample): It will be wrong.
How did QC-PCR, with all its flaws, become an acceptable HIV test?
Miller explains: "The way this situation has manifested itself in modern
science is like this: First some people spend a lot of time trying to
get this test to work, and if they're lucky, end up publishing papers
about caveats in the procedure. Second, others happen to get the test to
give them an answer that "makes sense" and publish their data as a
significant contribution to the field. Third, because of its relative
newness and arcane nature, it remains as quasi-accepted with many
passive sceptics and a few users. However, most who use it are more
interested in their own pet phenomenon than in the mechanics of the
reaction."
bDNA - BRANCHED DNA PCR
This is the test used in Ho's paper. Though it is not, strictly
speaking, PCR, it is referred to as such since it incorporates PCR-type
technology. The difference is that bDNA amplifies the signal, not the
target. That is, regular PCR makes more of the target so you can find
it, whereas bDNA sort of shines a bright spotlight on it so you can see
it better. Project Inform was kind enough to send me the following
explanation of how bDNA works: (9)
"Copies of a DNA probe are attached to the wall of a small laboratory
vessel; then the sample is put in. [A DNA probe is a small piece of DNA
complementary to the target DNA sequence.] This probe binds to a certain
part of HIV RNA, if it is found in the sample, holding the RNA in the
vessel. Then another DNA probe is put in; one end of this attaches to
another part of the HIV RNA. The other end of the second probe has many
branches and each branch ends with a "reporter" chemical that, under
certain conditions, will produce light, which can be detected by
laboratory equipment. Each molecule of HIV RNA can attach to one of
these branching structures and hold on to a small number of light
sources, not just one. In this way, very small amounts of the target RNA
can be detected, without the need for PCR amplification."
In his initial paper, Ho gave no data on the protocols for this test or
whether it was reliable. The reader was referred to two other papers
that were "in press". So, no data was available at that time to anyone
who wanted to verify this method. The data obtained from bDNA was
confirmed by QC-PCR, the details of QC-PCR being set out in a reference
authored by four co-authors of the Wei study, hardly what you might call
independent or objective researchers. In the tradition of HIV research,
unproven theories and faulty studies are accepted without question and
incorporated into the "conventional wisdom" before being properly
validated. By then, the damage is done, and if subsequent flaws are
discovered it hardly matters.
The mechanics of bDNA are complex: Five different hybridisation
reactions are going on. Hybridisation is a standard technique wherein a
DNA probe is put into a sample and will bind to any complementary
segments it finds. It's another indirect test, and it has a lot of
problems. According to molecular biologist Bryan Ellison, "The only time
molecular biology works is if you purify things first. There's always
the possibility of cross-reactions, especially when you put your probes
into a big soup of proteins" (which is exactly what the target blood
sample is).
Duesberg pointed out the following: After making the appropriate
adjustments to his calculations, Ho himself later found that more than
10,000 viruses inferred by the bDNA assay used in his Nature paper would
actually correspond to less than one infectious virus, leading one to
wonder what it is that is actually being measured on these tests. (10)
Yet these speculative and unvalidated papers have been accepted as
gospel truth!
In Ellison's mind, Ho's study is "Pure fantasy. There's never been a
paper that shows viral load."
The Problems With PCR
1. THE ACCURACY OF PCR HAS NEVER BEEN VERIFIED BY A PROPER GOLD STANDARD
To find out if any diagnostic test for HIV infection actually works, it
is necessary to verify the test with an independent gold standard. The
only proper gold standard for this purpose is HIV itself. In other
words, the results of your experimental test, whether it's PCR or
anything else, must be compared to the results of virus isolation in
each sample tested. If virus is actually found in each patient with a
positive PCR, and no virus is found in each patient with a negative PCR,
then you could say PCR is extremely accurate for detecting HIV.
The concept of virus isolation as a gold standard is particularly
important in the case of HIV, since HIV has been extremely difficult, if
not impossible, to define in genetic or molecular terms. Even if anyone
had ever accomplished virus isolation for HIV (11), it has never been
used as a gold standard for any HIV diagnostic test, including PCR. As
it stands right now, bDNA uses QC-PCR as a gold standard; QC-PCR uses
regular PCR as a gold standard; regular PCR uses antibody tests as a
gold standard, and antibody tests use each other. I have noticed time
after time that studies which are "verifying" an HIV antibody test will
invariably state that they evaluated the performance of their test on
samples which were known to be TRUE-POSITIVE or TRUE-NEGATIVE. How did
they know this? It's simple: Without a gold standard, they didn't.
It is sometimes argued that "studies have shown" these tests to agree
with each other or confirm each other's findings, and therefore they
must be correct. This is not rigorous scientific thinking. Sometimes you
can get the results of different tests to agree with each other, but
that does not prove anything -- no more than it would prove if five
criminals all agreed that they were somewhere else when the bank was
being robbed.
Eleopulos says the following about the importance of gold standards:
"The use of viral isolation as an independent means of establishing the
presence or absence of the virus is technically known as a gold
standard, and is a quintessential element for the authentication of any
diagnostic test. Without a gold standard, the investigator is hopelessly
disoriented, since he does not have an autonomous yardstick against
which he can appraise the test he is aspiring to develop.... Only by
this means can we assure patients that a positive HIV PCR is only ever
found in the presence of HIV infection, that is, the tests are highly
specific for HIV infection."
Even well-known AIDS researcher William Blattner has conceded that "one
difficulty in assaying the specificity and sensitivity of human
retrovirus assays (including HIV) is the absence of a final 'gold
standard.' In the absence of gold standards for both HTLV-1 and HIV-1,
the true sensitivity and specificity for the detection of viral
antibodies remain imprecise." (12)
Mark Craddock states QC-PCR is unverified and probably unverifiable. He
asks, "If PCR is the only way that the virus can be detected, then how
do you establish the precise viral load independently of PCR, so that
you can be certain that the figures PCR gives are correct?" All this has
apparently been lost on AIDS researchers, as it is regularly recommended
that PCR, particularly QC-PCR, be used as a gold standard for other HIV
tests. (9,13)
2. THE SPECIFICITY OF PCR HAS NEVER BEEN DETERMINED
Specificity means how often a test will give negative results in people
who are not infected. A test's specificity rating reveals the level of
false-positive results to expect when using that test. Without a virus
isolation gold standard, the true specificity will never be known. Even
using concordance with antibody tests as a gold standard, PCR was not
found to be very specific for HIV. (6 )
Citing a proficiency study involving five laboratories with extensive
PCR experience, Sloand states that the average specificity was 94.7%.
(14) Specificity was as low as 90%. Numbers in the 90s may sound good,
but in reality, this is not the case. The number of false-positives
compared to true positives is dependent on the prevalence of HIV
infection in any population being tested (15) -- the lower the
prevalence, the more false-positives.
Sloand comments that if the specificity levels achieved in this study
were applied to the potential blood donor population" (blood donors now
consisting of members of the low-prevalence general population), then
"...for every true silent infection detected, 1800 uninfected donors
would be classified as PCR positive and 3500 as PCR indeterminate. Thus
PCR is clearly not suitable for routine screening of transfused blood"
and by inference, any low-prevalence population. At a specificity of
90%, I would say it wasn't suitable for testing any population.
In a FAX I received from the Centers for Disease Control (CDC) in 1994
regarding PCR, they stated that "Neither its specificity nor its
sensitivity is known," and that "PCR is not recommended and is not
licensed for routine diagnostic purposes." (16)
In a nutshell, "The specificity of any form of PCR, for the HIV genome,
has not been determined." (5)
3. PCR PRIMERS ARE NOT SPECIFIC
According to Eleopulos, Turner, and Papadimitriou, "The minimum
requirement for [interpreting that a positive PCR signal, or
hybridisation in general, proves HIV infection] is prior proof that the
PCR primers and the hybridisation probes belong to a unique retrovirus,
HIV, and that the PCR and hybridisation reactions are HIV-specific."
Turner told me: "The PCR genomic arguments require isolation of HIV as
absolutely essential. Otherwise how does anyone know the origin of the
nucleic acid?"
Eleopulos disputes the reality of a distinct HIV genome. Conceding its
existence for the sake of argument, she offers the following evidence to
demonstrate PCR is nonspecific for HIV: (17)
* There is no way to be sure the "HIV" nucleic acid probes and PCR
primers are specific to HIV because: most, if not all, probes used for
hybridisation assays, including the PCR probes and primers, are obtained
from "HIV" grown in tissue cultures using cells (called a cell line)
taken from a patient with T4 cell leukemia, a disease which Gallo claims
is caused by a retrovirus similar to HIV -- HTLV-I. And recently a
retrovirus is claimed to have been isolated from a non-HIV-infected cell
culture using another cell line. Thus the standard cell lines used to
grow HIV have been shown to indicate other retroviruses. Since even the
well-established method for isolating retroviruses (which to date has
never been done for HIV) cannot distinguish one retrovirus from another,
one cannot be confident that "HIV" nucleic acid probes and PCR primers
are indeed specific for HIV.
* Proposed HIV genes hybridise with the structural genes of HTLV-I and
HTLV-II, two other human retroviruses. This means that if the probes
find genetic material from these other retroviruses, they will stick to
it and give a signal that they have found HIV instead. Since it is
accepted that 10% of AIDS-diagnosed patients carry HTLV-I and that the
normal human genome contains sequences related to HTLV-I and HTLV-II,
this type of cross-reaction can be anticipated.
* Normal human cells contain hundreds or thousands of retrovirus-like
sequences, that is, small stretches of DNA that match a small part of
the proposed genome of HIV or other retroviruses. And, since PCR often
amplifies just a small part of the entire genome of whatever it's
looking for, how do you know that what it finds isn't a normal cellular
gene sequence that just happens to match part of what's proposed for
HIV?
* Further evidence that PCR is nonspecific is that positive PCRs can be
obtained from cells without nucleic acids. So if there's no nucleic
acid, there's no DNA or RNA, and if there's no DNA or RNA, there's
certainly no HIV.
* The chemicals used in labs in the preparation of tissue cultures
(called buffers and reagents) may give positive PCR signals for HIV. (18
)
4. PCR DETECTS ONLY A SMALL FRAGMENT OF AN ENTIRE VIRUS
PCR detects at best single genes and most often, only bits of genes. If
PCR finds two or three genetic fragments out of a possible dozen
complete genes, this is not proof that all the genes (the entire genome)
are present. Part of a gene does not equal a complete virus particle.
HIV experts admit that the majority of proposed HIV genomes are
incomplete; they could never orchestrate the synthesis of a virus
particle.
Turner explains: "Even if all genomes were complete, having the plans
doesn't mean you've built the house. You can carry a whole retroviral
genome around inside your cells all your life without ever making a
virus particle." These two problems make it even more uncertain what the
significance of a positive PCR is.
5. THE FINDING OF "HIV RNA" ON PCR DOES NOT SIGNIFY THE PRESENCE OF HIV
These days, one keeps hearing the phrase "HIV RNA PCR." What's the
difference between that and regular old DNA PCR? Regular PCR looks for
the DNA version of what is often accepted to be the HIV genome; RNA PCR
looks for the RNA version, that is, free virus that has not infected a
cell.
With the new notion that HIV was busily replicating by the billions, it
was now thought necessary to find how much free virus there might be at
any given time. Free virus would contain only RNA, so if the PCR finds a
lot of "HIV RNA," it is believed billions of copies of free virus are
swarming around the patient's tissues. In other words, if you find RNA,
you've found HIV as well. Since it's believed HIV contains two strands
of RNA, the suggested formula is: Two RNAs = one virus.
In actuality, things are not this simple. In 1993, during the "HIV is
hiding in the lymph nodes" phase of the viral load theory, Piatak and
colleagues, including Shaw, admitted that in order to determine the
quantity of HIV particles, one must have prior evidence that the RNA
actually belongs to an HIV particle. (5) No such evidence was presented.
No relationship has yet been established between the amount of RNA and
the amount of particles that may or may not be present. And no one has
established whether the RNA comes from a virus particle or from
somewhere else. Without virus isolation, how do you know the origin of
the nucleic acid (RNA)?
6. CELL-FREE VIRUS IS NOT INFECTIOUS VIRUS
Even if Ho were right about billions of cell-free HIVs being present in
the bloodstream, free virus is by definition not infectious virus; it's
irrelevant as a pathogen. For HIV to infect a cell, its envelope
protein, gp120, must bind to the CD4 receptor site on the cell's
surface. However, as far back as 1983, Gallo pointed out that "the viral
envelope which is required for infectivity is very fragile. It tends to
come off when the virus buds from infected cells, thus rendering the
particles incapable of infecting new cells." Because of this, Gallo said
"cell-to-cell contact may be required" for retroviral infection. Since
gp120 is "crucial to HlV's ability to infect new cells," and since gp120
is not found in the cell-free particles, even if huge amounts of free
HIV are present in the blood, they would be non-infectious. (17)
7. PCR IS NOT STANDARDISED OR REPRODUCIBLE
In a recent paper, Teo and Shaunak commented on in situ PCR: "Despite
considerable effort, the technique is still technically difficult and
has not yet proved to be reliable or reproducible." (19)
In a study which compared PCR results to antibody test results, PCR was
found not to be reproducible and "False-positive and false-negative
results were observed in all laboratories (concordance with antibody
tests ranged from 40% to 100%)." (20)
8. PCR IS SUSCEPTIBLE TO CROSS-CONTAMINATION
Minute quantities of nucleic acids from prior specimens can easily
contaminate the specimen currently being tested, giving a false-positive
result. (21) Even microscopic bits of skin or hair from the lab
technician can cause this problem. Many sources of cross-contamination
exist, and it can occur "at any step in the procedure, from the point of
collection of samples through to the final amplification..." (22)
Other causes of false-positives are enumerated by Teo and Shaunak: "We
have now identified a number of factors which can contribute to the poor
amplification of the target DNA and to the generation of false-positive
signals. These factors include the effects of fixation, reagent
abstraction, DNA degradation, DNA end-labelling and product
diffusion.... We believe considerable caution should be exercised in the
interpretation of results generated using PCR in situ." (19)
9. FALSE-POSITIVES FREQUENTLY OCCUR WITH PCR
* A proficiency study to rate HIV PCR's performance on detecting
cell-free DNA showed "a disturbingly high rate of nonspecific
positivity" using the commonly employed primers (SK38/39, for the gag or
p24 gene). In fact, similar rates of positivity were found for both
antibody-negative and antibody-positive specimens (18% versus 26%)! (23)

* Out of 30 uninfected children, 6 had "occasional" positive PCR
results. (24)
* PCR performed on uninfected infants under one year of age showed 9/113
(9 out of 113), 15/143, 13/137, 7/87, and 1/63 infants to have positive
PCR tests. (25)
* Among 117 uninfected children born to HIV-infected mothers, six (5%)
had a false-positive PCR on cord blood. (26)
* In a PCR proficiency study, 54% of the laboratories involved had
problems with false-positive results; 9.3% of the total uninfected
specimens were reported as positive. (22)
* One out of 69 antibody-negative, non-seroconverters was PCR positive.
(27)
* A high-risk individual was initially PCR positive but negative on
repeat PCR testing of the same specimen by two different laboratories.
(27)
* The World Health Organisation's PCR working group demonstrated high
levels of false-positive results obtained during "blind" HIV PCR
studies. (22)
* Sheppard et al. stated in their study: "This trial demonstrated that
false-positive results, even with rigorous testing algorithms, occur
with sufficient frequency among uninfected individuals to remain a
serious problem." (28)
* Out of 327 health care workers exposed by needlestick to HIV, 4 had
one or more positive PCR results and 7 had indeterminate results. Later
samples for all 11 were negative and none seroconverted or developed p24
antigenemia, leading to the conclusion that "false-positive results
occur even under the most stringent test conditions." (29)
Conclusion
Essential to Dr. Ho's theory is the idea that HIV mutates so rapidly
that within days or weeks it has become resistant to whatever
"antiviral" drug the patient is taking. In order to prevent this, it is
recommended that the patient take three-drug "combos" which
theoretically hit HIV from all angles simultaneously, thus reducing the
chance that a resistant strain will survive. Meanwhile, one must
continuously monitor the "viral load" with tests that cost 200 bucks a
pop. Emphasis is placed on early intervention, that is, dose patients
with multi-drugs the minute they sero-convert (assuming that anyone
would know when this event took place to begin with) and keep them on
these drugs for the rest of their lives.
Even though no one has shown them to be accurate, viral load assays are
being vigorously promoted as state-of-the-art necessities for PWAs, and
it's not hard to figure out why. In the Washington Post (2-06-96), David
Brown inadvertently revealed the reason: "Aggressive HIV treatment will
probably be even more expensive than in the past. Measuring viral load
will cost about $200 per test, and the new generation of HIV medicines
will probably be at least as expensive as the ones they replace."
U. S. News and World Report (2-12-96) was more specific, estimating the
yearly cost of a protease inhibitor at around $6,000, and the cost of
triple-drug combinations at up to $12,000 to $18,000. Combos of three or
four drugs are now prescribed, where one (AZT) used to suffice. As more
and more drugs are considered necessary to "treat" people, many of whom
have nothing wrong with them, it is obvious what a cash cow this is
going to be for the pharmaceutical industry.
The viral load theory has created a new worry to produce unbearable
stress in the lives of desperate people. It is now said that a person
has only one shot at the new "anti-viral" drugs, chiefly the protease
inhibitors. If you don't take them at exactly the right time, in exactly
the right combinations or amounts, or if you foolishly take only one
drug at a time, or lower your dose because the current dose is making
you sick, your virus will become resistant and the drugs will never work
on you again. And you can't just quit the drugs either, for the same
reason, even if they are making you deathly ill.
Every article on the subject so far has a different expert guess about
how this whole program is supposed to work: no one knows if you can get
cured or merely hold the line; no one knows the long-term prognosis for
those who take this triple-toxic triple-combo. (Protease inhibitors have
produced extreme adverse reactions in many people, so it shouldn't be
hard to figure it out). Anyone foolish enough to sign up will become a
test animal for people who don't know what they're doing.
When will we stop allowing ourselves to be used as guinea pigs for
whatever crack-brained scheme comes down the pike? When will we put a
lock on our wallets and refuse to pay for the privilege of being
poisoned? And when will we quit supporting the most degraded human
beings in existence -- those who profit from the suffering of others?
Christine Johnson is a member of MENSA and a freelance science
journalist from Los Angeles, USA. She is the Contact person of HEAL/Los
Angeles, is on the Board of Advisors of Continuum magazine and
copy-editor of Reappraising AIDS. She has an extensive background in
medicine, law and library research and is motivated by a desire to find
out the truth about 'AIDS'. She has a special interest in making the
information in technical science journals accessible to the public. Over
the past four years she has followed the work of the Perth group and
written articles critical of the HIV antibody tests, including an
extensive interview with Eleni Papadopulos-Eleopulos, which have been
published world-wide.
References
1. Embretson J, Zupancicl M, Ribas JL, et al. 1992. "Massive covert
infection of helper T lymphocytes and macrophages by HIV during the
incubation period of AIDS." Nature. 362:359-362.
2. Pantaleo G, Graziosi C, Demarest J, et al. 1993. "HIV infection is
active and progressive in lymphoid tissue during the clinically latent
stage of disease." Nature. 362:355-358.
3. Ho DD, Neumann AU, Perelson AS, et al. 1995. "Rapid turnover of
plasma virions and CD4 lymphocytes in HIV-1 infection." Nature.
373:123-126.
4. Wei X, Ghosh SK, Taylor ME, et al. 1995. "Viral dynamics in human
immunodeficiency virus type 1 infection." Nature. 373:117-122.
5. Eleopulos E, Turner VF, Papadimitriou J. 1995. "Turnover of HIV-1 and
CD4 lymphocytes." Reappraising AIDS. 3(6):2-4.
6. Eleopulos E, Turner VF, Papadimitriou J. Letter to Nature. 1994. "Is
HIV really hiding in the Iymph nodes?"
7. Duesberg P, Bialy H. "Responding to 'Duesberg and the new view of
HIV"' in AIDS: Virus- or Drug-Induced. Kluwer Academic Publishers,
Boston (1996).
8. Craddock M. 1995. "HIV: Science by Press Conference." Reappraising
AIDS. 3(5):-4.
9. Project Inform Fact Sheet: PCR Tests. August 1, 1995.
10. Duesberg P, Bialy H. 1995. "HIV an illusion." Nature. 375:197.
11. Papadopulos-Eleopulos E, Turner VF and Papadimitriou JM. 1993. "Is a
positive Western Blot proof of HIV infection?" Bio/Technology.
11:696-707.
12. Blattner WA. 1989. Retroviruses. pp545-592. In Viral Infections in
Humans, third edition, edited by A Evans. Plenum Medical Book Company,
New York.
13. Macy E, Adelman D. 1988. Letter to New England Journal of Medicine.
December 15.
14. Sloand E, Pitt E, Chiarello R, et al. 1991. "HIV Testing: State of
the art." JAMA. 266:2861.
15. Maver, Robert. April 1993. "Testing AIDS Tests." Rethinking AIDS.
1(4):4.
16. Centers for Disease Control Faxback document #320320, January 1993.
17. Eleopulos E, Turner VF, Papadimitriou J, Causer D. 1995. "Factor
Vlll, HIV, and AIDS in hemophiliacs: An analysis of their relationship."
Genetica. 95(1-3):25-50.
18. Conway B. 1990. "Detection of HIV-1 by PCR in Clinical Specimens,"
p40-45, in Techniques in HIV Research, edited by A Aldovini and BD
Walker, MacMillan, New York.
19. Teo IA, Shaunak S. 1995. "PCR in situ: aspects which reduce
amplification and generate false-positive results." Histochem. J.
27:660.
20. Defer C, Agut H, Garbarg-Chenon A, et al. 1992. "Multicentre quality
control of polymerase chain reaction for detection of HIV DNA." AIDS.
6:659.
21. Bootman JS, Kitchin PA. 1994. "Reference preparations in the
standardization of HIV-1 PCR: An international collaborative study." J.
Vir. Meth. 49:1-8.
22. Bootman JS, Kitchin PA. 1992. "An international collaborative study
to assess a set of reference reagents for HIV-1 PCR." J. Vir. Meth.
37:23.
23. Busch MP, Henrard DR, Hewlett IK, et al. 1992. "Poor sensitivity,
specificity, and reproducibility of detection of HIV-1 DNA in serum by
polymerase chain reaction." J. AIDS. 5:872.
24. Garbarg-Chenon A, Segondy M, Conge A, et al. 1993. "Virus isolation,
polymerase chain reaction and in vitro antibody production for the
diagnosis of pediatric human immunodeficiency virus infection." J. Vir.
Methods. 42:117.
25. Paui MO, Tetali S, Lesser ML, et al. 1996. "Laboratory diagnosis of
infection status in infants perinatally exposed to human
immunodeficiency virus type 1." J. Inf. Dis. 173:68.
26. Simonon A, Lepage P, Karita E, et al. 1994. "An assessment of the
timing of mother-to-child transmission of human immunodeficiency virus
type 1 by means of polymerase chain reaction." J. AIDS. 7:952.
27. Celum CL, Coombs RW, Lafferty W, et al. 1991. "Indeterminate human
immunodeficiency virus type 1 Western Blots: Seroconversion risk,
specificity of supplemental tests, and an algorithm for evaluation." J.
Inf. Dis. 164:656.
28. Sheppard HW, Ascher MS, Busch MP, et al. 1991. "A multicenter
proficiency trial of gene amplification (PCR) for the detection of
HIV-1." J. AIDS. 4:277.
29. Gerberding JL. 1994. "Incidence and prevalence of human
immunodeficiency virus, hepatitis B virus, hepatitis C virus, and
cytomegalovirus among health care personnel at risk for blood exposure:
Final report from a longitudinal study." J. Inf. Dis. 170:1410.
With acknowledgements to: Paul Philpott, former research assistant in
immunology and current editor of Reappraising AIDS; and Todd Miller,
Ph.D. in biochemistry and molecular biology, of the University of Miami.
A similar version of this piece first appeared in the HEAL/New York
Bulletin, Oct. 1996

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