Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY
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Having been unable to refute anything of note recently, the Perth Group return to asking for "clarification" of various points. One cannot decide whether they are setting something up, or just unaware of the facts. But regardless:
(a) all AIDS patients are infected with "HIV";
Yes. That's not to say that all people with opportunistic infections will have HIV, any more than all such people will be taking anti-rejection drugs or be suffering from lymphomas, or have an inborne immune- deficiency... The only examples of "non-HIV AIDS" I have seen reported in the dissident literature have twisted the definition beyond its limits. I have posted previously here evidence showing HIV detection by serology, PCR and culture in 100% of AIDS patients and well over 90% of pre-AIDS complex (typically culture fails with very the low viral titres seen in some pre-AIDS patients). Serology may not be a "recognised standard for establishing the presence or absence of HIV-1 antibodies" but I wonder if the Perth Group have looked at the package inserts of any other diagnostic tests?
Additionally, I refer them to the fact that in several studies serology correlated 100% (or near as makes no difference) with virus culture, as I have repeatedly posted here. Most scientists would accept that serology DOES equate to HIV infection, and realise that the manufacturer is playing it safe as regards litigation. As an example, serology predicts the presence of absence of HIV by PCR to around 99% accuracy, and yet the same tests performed for CMV may only be 50-70% sensitive (with the PCR being the gold standard).
PCR-based assays should not be used for diagnosis in ADULTS, and I agree with the Perth Group on this. They are the only method of diagnosis in neonates, aside from culture (which is time consuming and labour- intensive). It seems a typical Perth Group trait to seek out statements regarding a situation and then apply them out of context. See my recent post regarding the antibody tests for some quotes regarding neonatal diagnosis specifically.
Since I have presented evidence that shows that 100% of AIDS patients have culturable HIV, then I cannot possibly conclude that "no proof exists for what percentage, if any, of AIDS patients are infected with "HIV"? " The problem lies not with the evidence, but the fact that the Perth Group refuse to accept it. The diagnostic criteria for HIV are extraordinarily stringent, compared to other diseases and even other infectious agents. A few scattered examples of sensitivity/specificity for typical diagnostic tests are: RSV: 90/93% CMV: 97/97% HSV: 88%/95% (up to 98/100% depending on the test) Flu: 45/99%
Which makes those quoted for HIV of (in one test used in Cambridge, UK) 97/100% rather good.
Can the Perth Group tell us all the standard by which HSV-2, an important STD, is judged? Is it any less or more than that of HIV? HIV serology has been confirmed by culture, PCR, lymph node biopsy and EM. As far as I can tell, the Gold Standard for HSV is western blot. HSV tests "may have extensive cross-reactivity" . HSV co-exists with many other kinds of STD including bacterial infections - who is to say that it isn't these that cause the vesicles? Aciclovir is an entirely non-specific antiviral that will readily chain-terminate non-viral DNA, and the infection is supposedly never cleared despite the disappearance of symptoms. Seroconversion may occur after the appearance of lesions, with a time of 25-47 days. How can the virus possibly be the cause of the vesicular lesions? One of the side effects of aciclovir is itching: how can this be distinguished from the itching of "herpes" infection?
Do the readers following along see how easy it is to state "truths" and create an argument from thin air to discredit something? Nothing I have said above regarding HSV is untrue, and is all easily verifiable online: why aren't the Perth Group attacking HSV as well as HIV?
(b) "HIV" kills the T4 cells;
This has been defunct as the primary cause of AIDS for at around 10 years. The current understanding, as I laid out in my recent posting which apparently went unread, is that HIV induces a state of chronic, abnormal, immune activation with concommitant cytokine skewing that prevents normal T cell replacement from the thymus. Immune deficiency is a result of cell death due to (in part) HIV killing, but probably more so apoptosis due to activation. T4 dysfunction leads to B cell and T8 cell dysfunction, the true effector cells of the specific immune response. This is why HIV results in AIDS after years rather than days of infection. The Perth Group have referenced several of the papers that lead to this conclusion: so their persistence in thinking that "HIV experts" think otherwise is confusing.
Immune activation not only leads to apoptosis (which would normally be replaced, in the absence of HIV) but also promotes HIV replication, which they may recall occurs preferentially in cells expressing NF-kB (i.e. activated lymphocytes and macrophages). This is taught at the undergraduate level as one of the feed-forward mechanisms HIV has for promoting its replication. It is neither overly complicated nor inconsistent.
HIV clearly kills cells in culture: presenting papers where workers have developed systems of long-term culture or used inactive T cells are hardly proof-positive that HIV isn't cytotoxic! Their interpretation of the data is lacking in understanding. I note again the obsession with the two initial protagonists in the HIV/AIDS story: researchers who have been one very minor part of the puzzle of HIV. Why do they ignore McMichael, Ho, Jackson, Hellerstein, Goedert, Chun, Mellors etc. Gallo indeed clearly states he thinks HIV is cytotoxic (Science. 1984 May 4;224(4648):500-3. "Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS.")
Once again I charge the Perth Group with putting words into researchers' mouths: at best grossly distorting the literature.
(c) decrease in T4 cells leads to the appearance of the clinical syndrome.
All the cohort evidence suggests that T4 decline precedes the clinical syndrome and the level of loss is predictive of the risk of an opportunistic infection. When I said that "AIDS-OI's" didn't require a low CD4 count, I wasn't referring to the syndrome, but isolated cases. Community acquired pneumonia in young people is unusual, but not worrying. 3 in a few months WOULD start alarm bells ringing.
The Perth Group also use the phrase "low CD4 (immune deficiency)" as if the two terms are synonymous. They must surely be aware that there are many forms of immune deficiency, not all of which will affect cellular immunity never mind CD4 T cells specifically.
If guns are not necessary for holes in the head, then any Perth Group member worth his salt must question the link between guns and holes in the head. I refer the Perth Group once again to the concept of "relative risk".
(d) T4 cell decrease is the "hallmark" and "gold standard" of HIV infection.
Hallmark yes, along with B cell hyperactivation and a reversal of the CD4/CD8 ratio. That's not to say that it's UNIQUE I rush to add (because the Perth Group are surely expecting that) but it is unusual without HIV. The decrease is also profound, and progressive: which excludes most conditions which produce similar profiles, such as ICL. The Cd4 T cell decline is seen in over 90% of HIV+ people: can the Perth Group find another cohort with a similar independant risk factor?
Gold Standard is a different concept: I would say that HIV infection is judged on a combination of factors and to label one as a gold standard to measure all others by is denying the progressive nature of the disease. I would personally accept lymph node culture as being one of the best standards by which to measure HIV infection (since it is so sensitive) but that may be positive in long-term noon-progressors, and therefore is of little significance to the health of someone who has CD4 counts of 800 perhaps. (That's not to say it's not of significance to a sexual partner of that person). In terms of rapid easy diagnostic surveillance, serology is by far the best diagnostic test. I therefore can't reply to this rather loaded question.
By their criteria, the Perth Group would have us throw out most of current medical knowledge it seems. I find it intriguing that as their arguments have been shut down they have shifted topic: in the past the Perth Group have argued that the "antigen exposures" of the AIDS risk groups are immunosuppressive [2-3], oxidative [3-6], and now immune stimulatory . When will they admit that perhaps they are, largely, irrelevant?
1.Field et al Pathology. 1993 Apr;25(2):175-9. The reliability of serological tests for the diagnosis of genital herpes: a critique.
2. Genetica 95: 25-50, 1995 FACTOR VIII, HIV AND AIDS IN HAEMOPHILIACS: AN ANALYSIS OF THEIR RELATIONSHIP
3. Continuum Magazine Volume 5 No. 5 1998/99. Pages 30-35
4. Medical Hypotheses No. 25, 151-162, 1988 Reappraisal of Aids: Is the Oxidation Induced by the Risk Factors the Primary Cause?
5. Res. Immunol. 1992, 143, 145-148 Oxidative Stress, HIV and AIDS
6. Letters to the BMJ Rapid Responses: http://bmj.bmjjournals.com/cgi/eletters/326/7387/495#78727
Competing interests: None declared