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Kaposi's sarcoma is more likely to develop in HIV-infected people who also have herpesvirus type 8 infection

Kaposi's sarcoma (KS) is the most prominent AIDS-defining cancer. Now scientists have discovered that human herpesvirus type 8 (HHV-8), a herpesvirus discovered in 1994, may actually be the causal agent for KS. According to recent findings from the Multicenter AIDS Cohort Study, there is strong evidence that, in addition to HHV-8 infection, other conditions (for example, a suppressed immune system) are necessary to cause KS. In fact, the risk of developing KS is increased if HHV-8 seroconversion (development of antibodies to HHV-8) occurs after a person becomes infected with the human immunodeficiency virus (HIV) that causes AIDS. The researchers tested for HHV-8 in the stored blood of 400 homosexual men with known dates of HIV-1 seroconversion (plus or minus 4.5 months).

The researchers compared times from HHV-8 seroconversion to KS for the 69 men who became infected with HHV-8 after acquiring HIV-1 to the 182 men who were HHV-8 seropositive before their HIV-1 infection. None of the men developed KS before coinfection with HIV-1. Men who developed HHV-8 antibodies after HIV-1 infection had more than double the risk of developing KS (risk ratio, 2.55) than men infected with HHV-8 before HIV-1. The risk of developing KS among HHV-8-infected men increased by 60 percent for each year of HIV-1 infection. Faster CD4 cell loss and higher HIV-1 RNA levels significantly predicted the more rapid development of KS in men acquiring HHV-8 after HIV-1.

HHV-8 probably remains latent in an immune-competent host in a way similar to that of other herpes viruses, cytomegalovirus, and Epstein-Barr virus. The lack of KS, despite infection with HHV-8 before HIV-1 infection supports this conclusion, explains lead author, Lisa P. Jacobson, Sc.D., of Johns Hopkins School of Hygiene and Public Health. She suggests that it may be the immunosuppression and possibly the stimulation of cytokines (proteins released in response to antigens) brought on by HIV-1 infection that promote the oncogenic process of HHV-8 (conversion of normal cells into cancer cells). Given the evidence that HHV-8 infection alone is not sufficient for the development of KS, there is little need to identify and closely monitor HHV-8-infected people, unless they are placed at further risk via a compromised immune system, conclude the authors. The Multicenter AIDS Cohort Study is cofunded by the National Institute of Allergy and Infectious Diseases, the National Cancer Institute, and the Agency for Healthcare Research and Quality.

For more details, see "Interaction of human immunodeficiency virus type 1 and human herpesvirus type 8 infections on the incidence of Kaposi's sarcoma," by Dr. Jacobson, Frank J. Jenkins, Ph.D., Gayle Springer, M.L.A., and others, in the June 2000 Journal of Infectious Diseases 181, pp. 1940-1949.

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