PURPOSE: There is notable heterogeneity in the progression to Kaposi's sarcoma (KS) among men coinfected with HIV-1 and human herpesvirus type 8 (HHV-8); additional determinants of KS likely exist. Here, we explore sexual activity as a proxy for a sexually transmitted determinant beyond HIV-1 and HHV-8. METHODS: The association between sexual activity and incident KS was estimated with data from 1354 HIV-1- and HHV-8-coinfected homosexual men who were followed for up to 10 years in the Multicenter AIDS Cohort Study. RESULTS: As expected, white race, low CD4 cell count, and the acquisition of HHV-8 after HIV-1 infection increased, whereas smoking decreased, the hazard of KS. The unadjusted hazard of KS among those with high sexual activity was 0.68 relative to the hazard of those with low sexual activity (95% confidence interval, 0.49-0.93) and was somewhat muted after adjustment for characteristics measured at study entry (i.e., race, smoking, CD4 cell count, infection order, history of sexual activity, and sexually transmitted diseases). However, adjustment for time-varying covariates, particularly CD4 cell count, resulted in a nullification of the association (adjusted hazard ratio = 1.06; 95% confidence interval, 0.77-1.48). CONCLUSION: Once HIV-1 and HHV-8 coinfection is established in homosexual men, progression to KS does not appear to be caused by a third pathogen transmitted by sexual activity.
PURPOSE: There is notable heterogeneity in the progression to Kaposi's sarcoma (KS) among men coinfected with HIV-1 and humanherpesvirus type 8 (HHV-8); additional determinants of KS likely exist. Here, we explore sexual activity as a proxy for a sexually transmitted determinant beyond HIV-1 and HHV-8. METHODS: The association between sexual activity and incident KS was estimated with data from 1354 HIV-1- and HHV-8-coinfected homosexual men who were followed for up to 10 years in the Multicenter AIDS Cohort Study. RESULTS: As expected, white race, low CD4 cell count, and the acquisition of HHV-8 after HIV-1infection increased, whereas smoking decreased, the hazard of KS. The unadjusted hazard of KS among those with high sexual activity was 0.68 relative to the hazard of those with low sexual activity (95% confidence interval, 0.49-0.93) and was somewhat muted after adjustment for characteristics measured at study entry (i.e., race, smoking, CD4 cell count, infection order, history of sexual activity, and sexually transmitted diseases). However, adjustment for time-varying covariates, particularly CD4 cell count, resulted in a nullification of the association (adjusted hazard ratio = 1.06; 95% confidence interval, 0.77-1.48). CONCLUSION: Once HIV-1 and HHV-8 coinfection is established in homosexual men, progression to KS does not appear to be caused by a third pathogen transmitted by sexual activity.
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