To quote, for example, from an article in Immunology Today 1998 Vol.19 p 10-17 entitled "HIV-induced decline in blood CD4/CD8 ratios: viral killing or altered lymphocyte traffiking?" :
"During HIV infection CD4 cell numbers and CD4/CD8 ratios decline in the blood. This is usually attributed to direct viral killing or to other indirect mechanisms. However, current models generally assume that such changes in the blood are representative of changes in total CD4 cell numbers throughout the body. This article discusses the importance of alterations in CD4 and CD8 cell migration in regulating blood lymphocyte levels and questions the extent of virus mediated CD4 cell destruction"
To also quote from Roederer, Nature Med. Vol 4 p145:
"In this issue of Nature Medicine, reports by Pakker et al and Gorochov et al provide the final nails in the coffin for models of T-cell dynamics in which a major reason for changes in T-cell numbers is the death of HIV infected cells"
Although there is a shortage of studies examining the effects of antiretroviral drugs upon CD4 cells, what we do have provides grounds for saying that they definitely do destroy CD4 cells. AZT has been found in several studies to be toxic to CD4 cells (Balzarini et al. Journal of Biological Chemistry Vol. 264, pp 6127-6133, 1989; Mansuri et al. Antimicrobial Agents and Chemotherapy Vol. 34, pp637-641, 1990; Hitchcock et al. Antiviral Chemistry and Chemotherapy, Vol 2, pp 125-132, 1991.) An independent study showed that AZT is about 1000-times (!) more toxic for human T-cells in culture (at about 1 µM concentration) than the study conducted by its manufacturer and the NIH concluded (Avramis et al, AIDS, Vol. 3, pp 417-422). Lymphocyte counts decreased significantly in humans treated with AZT but not in untreated controls (Richman et al, NEJM, Vol. 317 pp 192-197, 1987) Another study found that AZT users experienced more rapid CD4 cell depletion than those not on antiretrovirals (Alcabes et al, American Journal of Epidemiology, Vol. 137, pp 898-1000, 1993). Didanosine (ddI or Videx), is listed in the Physician's Desk Reference (1999) as causing serious levels of "leukopenia" which involves reductions of all white blood cells including lymphocytes in 13% to 16% of users.
In the June 2, 2002 issue of the Journal of Virology, researchers report that the protease inhibitor drugs Crixivan (indinavir) and Invarase (saquinavir) caused T cell death in healthy HIV negative donor blood in three separate experiments: http://healtoronto.com/tcelldeath.html
The idea with evolution by natural selection is that organisms improve themselves by random mutations preserved by natural selection. So, if a mutation confers an advantage it is preserved and the organism is optimised for survival. When mutations confer a disadvantage they are selected against because the organism carrying this unfortuate mutation cannot persist in the population. If we are talking about HIV as a viable biological entity then always the fittest virions will comprise the greatest proportion of any particular HIV population. Natural selection dictates that beneficial mutations are PRESERVED. The basic message is that viral populations can tolerate "high" levels of mutation as long as they are not so high that beneficial mutations cannot be preserved in the majority of the viral population.
We are being asked to believe that HIV is so prone to mutation as to become simultaneously resistant to a combination of 3 anti-retroviral agents and that despite this level of mutation HIV can still sustain itself as a pathogenic virus.
If we assume that HIV does not mutate to an extent that renders it naturally harmless (it is harmless anyway) then it will have optimised its activity through natural selection. When exposed to an unnatural inhibitor designed to block its HIV protease, the protease will mutate to become resistant but because of the high precision required of the protease in its function, infectious HIV cannot be produced. To quote Dr David Rasnick from the article I posted on virusscience.org:
"Since the wild-type HIV protease has evolved to the optimal level of activity, virtually all alterations to the enzyme’s structure that affect catalytic efficiency are lethal to the virus. Mutations of the protease that reduce inhibitor binding result in an even more profound reduction in catalytic activity. This is because the overall catalytic efficiency of a mutant HIV protease is given by the product of the relative efficiencies of the mutant enzyme with respect to the wild-type for all eight obligatory cleavages (28) . These eight cleavages can be thought of as an eight-number combination lock. Not only does HIV protease have to make all eight cleavages, but the enzyme must do it in the right order. Therefore, even in the absence of inhibitors, the inhibitor-resistant mutant HIV proteases do not lead to viable, infectious virus."
For futher details you are referred to the Journal of Biological Chemistry, 1997, Vol. 272, p 6348-6353.
The viral load test relies upon a technique called PCR, the Polymerase Chain Reaction. For the “viral load” PCR which supposedly picks up the HIV genome, which is RNA not DNA, the initial step must be reverse transcription of the "HIV RNA" to DNA. This is because the reaction uses a heat resistant DNA polymerase enzyme called taq polymerase. There are no heat resistant RNA polymerases. The idea with PCR as it is applied to HIV is that within a collection of genetic fragments from an HIV positive person PCR will home in on HIV, specifically multiplying only that RNA (as complementary DNA). The idea is that the PCR amplification is used as an extraction procedure. This is done because they have no other way of detecting the “HIV”. The problem with this, according to Kary Mullis who won the 1993 Nobel Prize for inventing PCR, is that PCR is too efficient and multiplies everything not just the intended target.
PCR works as follows: double stranded DNA is separated into its single strands, complementary base pair primers are added which bind on one end of each DNA strand. This arrangement acts as a template for an enzyme called DNA polymerase to go from the primer along each strand constructing a complementary strand as it goes. The idea is that if the primers used are complementary to the ends of the target DNA they will only bind to that target DNA and this binding will initiate complementary strand construction by DNA polymerase. So after many cycles of this we get enormous amplification of only a specific DNA sequence.
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.
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 so abundant? Traditional methods should suffice. Both of these PCR techniques are fundamentally flawed.
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. Yet Ho’s speculative and unvalidated papers have been accepted as gospel truth! To quote from p203 of the Ho paper NEJM 1995 Vol. 332 p201-208: "Plasma cultures were uniformly negative for infectious virus in tests of 9 subjects involving up to 1ml of sample. However, particle-associated HIV-1 RNA was detected in 4 subjects by an ultrasensitive branched DNA assay, the values ranged from 839 to 11,549 copies of RNA per millilitre of plasma." We also read that the viral load test overestimates functional HIV by a factor of 60,000 on average (see Science 1993, Vol.259 p1749-1754).
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” (which is exactly what the target blood sample is). In Ellison’s mind, Ho’s study is “Pure fantasy. There’s never been a paper that shows viral load.” PCR is done on supposedly cell free extracts obtained from density gradient centrifugation but the notion that these extracts contain only viral RNA, indeed only HIV RNA, and no cellular material is wrong. 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. 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. Even using concordance with antibody tests as a gold standard, PCR was not found to be very specific for HIV. There are many cases of positive PCRs in HIV negative people. The PCR primers are not HIV specific. Normal human cells contain hundreds or thousands of retrovirus-like sequences.
HIV experts admit that the majority of proposed HIV genomes are incomplete; their expresssion could never result in the synthesis of a virus particle. PCR only picks up parts of viral genomes, at most single genes.
The idea with QC-PCR is that control DNA, a known amount of test DNA (similar to “HIV” but identifiably different) and the “HIV” DNA are amplified together. If the relative amounts of control DNA and test DNA remain the same then you can look at the final number of test DNA copies, compare it with the known number of test DNA fragments at the start, use this to get your amplification factor and then divide the number of amplified “HIV” copies by this factor to get the “viral load”. In practice the relative amounts of control and test DNA do not remain the same but AIDS Inc. don’t care.
I am informed that for the HIV-1 Amplicor PCR (Roche), the specimen is amplified, according to the package insert, initially through 4 cycles and then through an additional 26 cycles at slightly different temperatures. The PCR reaction is not a sustained exponential increase, it starts to plateau at around 0.1 billion copies. According to the literature with 12 to 400 starting copies 30 cycles are needed to ensure sufficient sensitivity of detection. Since we need a measurable amount of test DNA to start with, the test DNA will start to plateau before the “HIV” DNA does, leading to an inflated estimate of “viral load”
Studies showing that AIDS occurs in the absense of all other possible non-HIV causal factors.
Prevalence of positive “viral load” in HIV negatives at risk for AIDS and with “AIDS like” illnesses.
Comparison of CD4 counts over a long period between a group of HIV negatives and a group of healthy, heterosexual HIV positives who lead a healthy lifestyle (do not take recreational drugs, anti-HIVdrugs etc.).
Apart from the early fraudulent AZT trials and the damning Concorde study (172 participants died, 169 while taking AZT, 3 while on placebo) all studies of drug efficacy compare drugs with drugs, there are no unmedicated controls.
Perfectly healthy people have been pushed onto the combos either as a result of the “hit hard, hit early” doctrine or as a result of indirect markers like viral load and CD4 count. There is no comparison of survival times in developed countries of healthy HIV+ heterosexuals who lead a healthy lifestyle and were not given combos for either of these reasons, with those in the same group who were given them for these reasons.
In the early days of the HIV era a small group of virologists to which everyone deferred stated as fact that HIV causes AIDS by directly destroying CD4 cells, although there was no evidence for this at the time. When there was still no evidence, rather than follow the scientific method and consider the importance of other factors, it was confidently stated as fact that HIV instead causes AIDS by INDIRECTLY destroying, or indirectly reducing, the number of CD4 cells. True to form, there is still no evidence to clarify this position. Even after receiving mind bogglingly huge research funding for over 20 years HIV “scientists” still do not have the evidence to show how HIV can cause AIDS.