Risk factors for human herpesvirus 8 seropositivity in the AIDS Cancer Cohort Study

BackgroundCigarette smoking has been associated with a decreased risk for AIDS-related and classical KS, but whether it is associated with decreased risk of human herpesvirus 8 (HHV-8) infection is unknown.Study designWe evaluated factors associated with HHV-8 seropositivity in 2795 participants (132 with KS) in the National Cancer Institute AIDS Cancer Cohort, including 1621 men who have sex with men (MSM), 660 heterosexual men and 514 women. Odds ratios (OR) and 95% confidence intervals were estimated using logistic regression models.ResultsAmong non-KS subjects, HHV-8 seropositivity was 6%, 13% and 29% among women, heterosexual men and MSM, respectively. HHV-8 seropositivity was decreased in heavier (≥1/2 pack/day) compared to lighter smokers among women (5% versus 8%; adjusted OR (aOR) 0.4; 95% CI 0.2–0.8) and MSM (27% versus 32%; aOR 0.7; 95% CI 0.6–1.0), but not among heterosexual men (12% versus 16%; aOR 0.7; 95% CI 0.4–1.2). HHV-8 seroprevalence was increased in heavier (≥1 drink/day) compared to lighter consumers of alcohol among women (16% versus 4%; adjusted OR 5.2; 95% CI 2.3–12), but not among MSM (33% versus 28%; aOR 1.2; 95% CI 0.9–1.6) or heterosexual men (13% versus 13%; aOR 1.1; 95% CI 0.6–2.0). In analyses adjusted for smoking and drinking, HHV-8 seropositivity was positively associated with chlamydia infection (OR = 4.3; 95% CI 1.2–13) and with marital status among women pheterogeneity = 0.03, and with hepatitis (OR = 1.6; 95% CI 1.2–2.1), gonorrhea (OR = 1.5; 95% CI 1.1–1.9), genital warts (OR = 1.5; 95% CI 1.1–2.0) and nitrate inhalant use (OR = 1.7; 95% CI 1.3–2.3) among MSM.ConclusionsInverse association of HHV-8 seropositivity with cigarette smoking may indicate protective effect of tobacco smoke on HHV-8 infection, whereas positive associations with alcohol may reflect either behavioral factors or biological effects modulating susceptibility. Smoking and drinking may influence KS risk, at least in part, by altering the natural history of HHV-8 infection.