KS risks. 21 July 2004
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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY

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Re: KS risks.

James Whitehead makes an important point regarding KS, in that the HIV-positive population is far more heterogenous that it was originally, and so it was with this in mind that I set about updating my KS facts!

As many will be aware, KS and PCP (pneumocystis carinii pneumonia) were the two original OIs described in New York and San Francisco at the start of the HIV epidemic in the USA. Both cohorts were young homosexual men. I'm fairly sure that my original figure of 33000 was based upon a homosexual cohort from the early days of AIDS investigation.

Older analysis from the US states that the annual incidence of Kaposi's sarcoma in the United States was 0.02 to 0.06 per 100,000 population (source NIH, dated 1962 http://www.niaid.nih.gov/publications/hivaids/all.htm ). In the 1980s KS was the AIDS-defining illess in approxmiately 20-30% of people (30,000 per 100,000). If anything 33,000-fold increased risk might be an underestimation! (but these are overall risk rates, not annual incidence...)

However, HIV has spread beyond the original homosexual risk group, in particular to the heterosexual, hemophiliac and drug use groups. For whatever reason, these are far less likely to harbour the HHV8 virus: some studies I've seen have said that the single significant risk of transmission is anal intercourse. Clearly if the HHV8 risk factor isn't moving much but the HIV risk factor is, the overall risk of getting KS will decline. As of 2003 the relative risk seems to be 100-300 fold which seems rather low (Source The Body http://www.thebody.com/cfa/rita_summer03/cancer_hiv.html and references within). Without pulling up the original references it's hard to add caveats or further explanations, but one caveat may be improved treatment, which has been shown to reduce the incidence of KS by over 90%. ( http://www.thebody.com/kaiser/2004/may12_04/kaposis_sarcoma.html )

It is entirely true that KS is seen in transplant recipients (not just kidney). There are four types of KS: transplant related (indeed caused by the immunosuppressive drugs, usually relatively benign), Mediterranean (seen in elderly men in that geographical area, often on the legs), African (quite common, may be endemic in certain areas) and AIDS-KS (can be rather nasty, with lung involvement and death). HHV8 can be detected in all samples of all types of KS and HHV8 has proven oncogenic genes within it. For whatever reason normal immune surveillance can control its effect on lymph vessel cells (those that eventually become KS).

I found a reference that states "The overall incidence of Kaposiís sarcoma after organ transplantation is 0.52%, 150-200 times more frequent than the general population" (Ganem D.: KSHV and Kaposiís sarcoma: the end of the beginning? Cell 91: 157-60,1997. referenced from http://www.biotrin.ie/lab/HHV/hhv8/ ). This is clearly a lot lower than that of untreated AIDS patients, but still significant.

I have read reports of transient p24 antigen detection is transplant recipients and people with Lupus. My bet is that this is an activation of an endogenous retrovirus (HERV) with a mild antigenic overlap with HIV. Certainly antibodies to HERVs can be produced, and may be why people given high doses of immunoglobulin show transient ELISA positive results to HIV. A brief BLAST alignment of a HERV K sequence (the most active HERV) and HIV-1 however gives "no significant similarity". Same result for a specific alignment of the Gag (containing p24) proteins. So much for that theory ;-) I guess I'll remain none-the-wiser as to the cause of that. p24 isn't a very good marker of HIV anyway - a high percentage (30-50% I believe in some studies) of HIV+ people have no detectable p24 antigen in peripheral blood.

Competing interests: None declared