Background and objectives: Genital ulcer disease (GUD) is a major risk factor for human immunodeficiency virus (HIV) transmission. Cross-sectional studies have suggested that HIV infection may itself predispose to genital ulceration (GU).
Goal: To prospectively study the effects of HIV type 1 (HIV-1) infection and behavioral variables on GU incidence.
Methods: A cohort of 302 Kenyan female sex-workers was established in April 1991. Women were scheduled for assessment every 2 weeks, and bloods were collected every 6 months for HIV serology, rapid plasma reagin (RPR) and CD4 counts. Logistic regression was used to study risk factors for incident genital ulcers.
Results: 189 women (62.5%) had at least one incident ulcer over 24.3 +/- 15.3 months. GU incidence was higher in seropositive than initially seronegative women (82% vs. 48%; odds ratio [OR]) = 4.33; P < 0.01). Only HIV-1 seropositivity (OR = 3.42), a CD4 count < 200/ml (OR = 1.94), and oral contraceptive use (OR = 1.35) were associated (P < 0.05) with GU incidence in regression analysis. For those ulcers where an etiology was actively sought, Hemophilus ducreyi was confirmed in 54 (19%) of cases, and syphilis in 30 (29%).
Conclusion: GU incidence in Kenyan sex workers is independently affected by HIV-1 serostatus, degree of immunosuppression, and oral contraceptive use.
PIP: Both cross-sectional and prospective studies in Africa have revealed an association between genital ulcer disease (GUD) and HIV-1; it is unclear, however, which of these infections facilitates the other. The epidemiology of GUD was investigated in a prospective cohort study of 302 female sex workers from a slum area in Nairobi, Kenya. At study intake in 1985, 157 women (52%) were HIV-1 seropositive. After a mean follow-up duration of 27.2 months, 36 (25%) initially HIV-negative women seroconverted. 189 women (62.5%) had at least 1 incident ulcer in the follow-up period and a total of 541 new cases were diagnosed. GUD incidence was significantly higher in HIV-positive women (82%) than initially seronegative women (48%). The mean number of new genital ulcerations recorded during the follow-up period was 1.8 (2.7 in initially seropositive women and 1.0 in initially seronegative women). The only significant risk factors for GUD incidence in the regression analyses were HIV-1 seropositivity (odds ratio (OR), 3.42), a CD4 count under 200/ml (OR, 1.94), and oral contraceptive use (OR, 1.35). The significant increase in GUD incidence observed relatively soon after primary HIV infection among the 36 seroconverters strongly suggests that HIV-1 itself plays a causal role in the etiology of genital ulcers. Moreover, the finding that the duration of prostitution was negatively associated with the incidence of ulcers in HIV-negative but not HIV-positive women implies that HIV-1 infection may attenuate the acquisition or retention of effective immune responses against the etiologic agents of GUD.