Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY
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Christopher Tyler's eloquent exposition puts forward some cogent points. No-one is saying that HIV alone is responsible for causing all forms of immune suppression, as he points out when quoting the CDC AIDS definition.
What is missing however is the fact that these issues have already been addressed. HIV infection is the only independant predictive factor for the classic AIDS-defining conditions. Regardless of the laboratory findings of popper exposure, it fails to explain why all KS lesions from all four types of KS, including AIDS-KS, contain HHV8. It also fails to explain why HIV antibodies (which correlate with virus culture and PCR - standards far in excess of those expected of other pathogens) correlate with a massively increased risk of opportunistic infections independantly of other factors.
For example alcohol is a drug known to cause mild immunosuppression, and yet did not contribute to CD4 T cell loss in HIV+ people.  Studies of intravenous drug users also show CD4 T cell decline independant of drug use and only occurring after HIV seroconversion . I find it extremely hard to refute that kind of evidence.
The issue of poppers in KS has been addressed several times. Ascher et al found no correlation between popper use and risk of AIDS, independant of HIV infection. . Others have found that they may have an effect IN ADDITION TO HIV infection  and of course the use of poppers during a sexual act that could transmit HHV8, found in all forms of KS, is a reasonable hypothesis! It should be noted that the strongest literature in support of the link between poppers and KS is prior to the knowledge that a previously unknown virus was being transmitted during the sexual acts associated with poppers. Such an effect is known as confounding. For example, one study showed a 7-fold higher risk of HHV8 infection in those who used poppers compared to those who didn't.  Whether this is behavioural or due to poppers transiently lowering the immune system such that infection is more likely doesn't really matter - it doesn't detract from the fact that it is the underlying HHV8 infection that is responsible for KS.
In contrast to Mr Russell's claim that KS has nothing to do with sexual transmission, this data shows just the opposite. It is true that bisexuals and homosexual IV drug users who shared needles were thought to lead to a heterosexual explosion in HIV infection. This has in fact been shown to happen, but on a much smaller scale than expected. It doesn't mean it doesn't happen (small does not equate to non-existant!) only that the original estimates were wrong and that, in my opinion, the public health message got across before widespread cross-risk group transmission occurred. 
The longitudinal studies are the strongest evidence, to me, of the causative role of HIV. Several of these follow cohorts of people prospectively, and note the time of seroconversion. It is only after this point that CD4 T cells decline. The importance of these kind of studies is that the other cohort members who are presumably exposed to the same risk factors other than HIV infection do not show this. Some examples of comparisons between HIV+ and HIV- individuals, or longitudinal demonstration of CD4 T cell declines are below [2, 7-14]. Reference 14 is especially important because it includes data for several years PRIOR to seroconversion, rather neatly refuting any and all attempts to suggest that lifestyle or drug use act to cause the immune deficiency seen in AIDS.
There is a wealth of information showing that HIV infection precedes a specific immune decline. This is not something one would even expect with a relatively non-specific insult like drug toxicity. Of course other factors will contribute, and this is a recurring theme in the literature. Some may contribute to predisposition to HIV infection, some to rate of progression. Mr Tyler may be right in that these factors may have been relatively neglected compared to HIV, in this era of antibiotics and antivirals.
It should not be forgotten that HIV is itself an infection, and those with weaker immune systems are likely to be worse affected (e.g. there is a clear age-related effect, with the very young infants and the older adults progressing to AIDS faster than young adults). A combination of damaging events may result in an outcome far worse than a simple additive effect - this is why there is so much literature investigating potential co-factors.
Nick Bennett firstname.lastname@example.org
1. Crum et al Alcohol Clin Exp Res. 1996 Apr;20(2):364-71."Alcohol use and T-lymphocyte subsets among injection drug users with HIV-1 infection: a prospective analysis."
2. Margolick et al JAMA. 1992 Mar 25;267(12):1631-6. "Changes in T- lymphocyte subsets in intravenous drug users with HIV-1 infection."
3. Ascher et al Nature. 1993 Mar 11;362(6416):103-4. " Does drug use cause AIDS?" and subsequent letters.
4. Archibald et al Epidemiology. 1992 May;3(3):203-9. "Evidence for a sexually transmitted cofactor for AIDS-related Kaposi's sarcoma in a cohort of homosexual men."
5. Casper et al J Infect Dis. 2002 Apr 1;185(7):990-3. Epub 2002 Mar 11."Correlates of prevalent and incident Kaposi's sarcoma-associated herpesvirus infection in men who have sex with men."
6. Winkelstein et al Am J Public Health. 1988 Nov;78(11):1472-4. "The San Francisco Men's Health Study: continued decline in HIV seroconversion rates among homosexual/bisexual men."
7. Goedert et al. Science. 1986 Feb 28;231(4741):992-5. "Three-year incidence of AIDS in five cohorts of HTLV-III-infected risk group members."
8. Jaffe et al. Ann Intern Med. 1985 Aug;103(2):210-4. "The acquired immunodeficiency syndrome in a cohort of homosexual men. A six- year follow-up study."
9. Goedert et al. Eur J Epidemiol. 1985 Sep;1(3):155-9. "Epidemiological evidence that HTLV-III is the AIDS agent."
10. Goedert et al. N Engl J Med. 1989 Oct 26;321(17):1141-8. "A prospective study of human immunodeficiency virus type 1 infection and the development of AIDS in subjects with hemophilia."
11. Knutsen et al Ann Allergy. 1989 Sep;63(3):189-94. "Decrease of CD4 cell number and function in HIV-seropositive hemophiliacs in a longitudinal study."
12. Cuthbert et al BMJ. 1990 Oct 27;301(6758):956-61. "Five year prospective study of HIV infection in the Edinburgh haemophiliac cohort."
13. Chaisson et al J Acquir Immune Defic Syndr. 1992;5(5):456-60. "Immune serum markers and CD4 cell counts in HIV-infected intravenous drug users."
14. Margolick et al J Acquir Immune Defic Syndr. 1993 Feb;6(2):153- 61."Changes in T and non-T lymphocyte subsets following seroconversion to HIV-1: stable CD3+ and declining CD3- populations suggest regulatory responses linked to loss of CD4 lymphocytes. The Multicenter AIDS Cohort Study."
Competing interests: None declared