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EXUALLY TRANSMITTED INFECtions (STIs) are important cofactors in the human immunodeficiency virus type 1 (HIV-1)/AIDS pandemic. In HIV-infected individuals, not only may symptomatic and asymptomatic STIs enhance sexual transmission of HIV-1 by increasing virus shedding from the genital tract, 1-3 but at the same time HIV-1 infection itself increases susceptibility to STIs. 4 There is also considerable evidence that STIs may increase HIV-1 susceptibility in uninfected individuals, 5,6 although differentiating cause from effect is more difficult in this situation. 7 Prevention or control of STIs as a strategy for preventing HIV-1 transmission has met with mixed success. Improved syndromic management of STIs reduced HIV-1 incidence in com-munities in Mwanza, Tanzania, 8 but in Uganda neither a similar strategy nor antibiotic mass-treatment of whole communities had an impact on HIV-1 Author Affiliations and Members of the Kibera HIV Study Group are listed at the end of this article.

Among 302 female sex workers in Nairobi, Kenya, who were followed for 17.6 +/- 11.1 months, 146 had one or more infections with Chlamydia trachomatis; 102 had uncomplicated cervical infection only, 23 had C. trachomatis pelvic inflammatory disease (PID), and 21 had combined C. trachomatis and Neisseria gonorrhoeae PID. As determined by multivariate logistic regression analysis, risk factors for C. trachomatis PID included repeated C. trachomatis infection (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.3-2.4; P = .0004), antibody to C. trachomatis heat-shock protein 60 (OR, 3.9; CI, 1.04-14.5; P = .04), oral contraceptive use (OR, 0.28; 95% CI, 0.08-0.99; P = .048), and number of episodes of nongonococcal nonchlamydial PID (OR, 1.7; 95% CI, 1.1-2.7; P = .02). Among human immunodeficiency virus (HIV)-seropositive women, a CD4 lymphocyte count of <400/mm3 was an additional independent risk factor for C. trachomatis PID (OR, 21.7; 95% CI, 1.2-383; P = .036); among HLA-typed women, HLA-A31 was independently associated with C. trachomatis PID (OR, 5.6; 95% CI, 1.1-29.4; P = .043). The results suggest an immune-mediated pathogenesis for C. trachomatis PID.

We compared the prevalence of antibody to Chlamydia trachomatis among 88 women undergoing an evaluation for infertility and 49 women attending an antenatal clinic. Demographic data regarding sexual behavior were also collected. Eighteen women had tubal infertility and 70 had infertility due to a variety of other reasons. In comparison with women who had other causes for infertility, women with tubal infertility began coitus sooner (17.7 +/- 2.2 years vs. 19.5 +/- 3.4 years, P less than .05) and had more lifetime sex partners (4.5 vs. 1.33, P less than .001). Women with tubal infertility had a higher prevalence of antibody to C. trachomatis (13 of 18) than did women with nontubal causes for infertility (6 of 70, P less than .0001) or pregnant women (11 of 49, P = .0003). This high prevalence of antibody to C. trachomatis among women with tubal infertility was independent of sexual experience. By immunoblot analysis, an antigen of approximately 57,000 Da was immunodominant in 11 of 13 seropositive subjects with tubal infertility vs. 2 of 6 seropositive subjects with nontubal infertility (P = .046) and 1 of 11 seropositive pregnant women (P = .0003). Thus, women with tubal infertility frequently have serological evidence of prior infection with C. trachomatis and have a distinctive antigen-specific humoral immune response. These results further support the etiologic role of infection with C. trachomatis in tubal infertility.

Female sex workers in Nairobi were prospectively evaluated for risk factors of incident Chlamydia trachomatis infection. Independent risk factors included cervical ectopy (P=.007), gonococcal infection (P=.002), human immunodeficiency virus (HIV) seropositivity (P=.003), HIV seroconversion (P=.001), and duration of prostitution (P=.002). Eighteen different C. trachomatis outer membrane protein (omp1) genotypes were identified, with the allelic composition of the C. trachomatis population changing significantly over time (P=.005). Seventeen of 19 reinfections > or = 6 months apart were with different C. trachomatis omp1 genotypes. Women with HIV infection had an increased proportion of visits with C. trachomatis infection (P=.001) and an increased risk of reinfection (P=.008). Overall, the data demonstrate significant fluctuations in the genotype composition of the C. trachomatis population and a reduced rate of same-genotype reinfection consistent with the occurrence of strain-specific immunity.

We tested 174 bovine microsatellite primer pairs for use in a primitive breed of sheep and two species of deer. Of 173 markers, 127 (73.4%) gave a product in Soay sheep (Ovis aries) of which 54 (42.5%) were polymorphic. One hundred and twenty-nine of 174 (74.1%) markers gave a product in red deer (Cervus elaphus) of which 72 (55.8%) were polymorphic. In sika deer (Cervus nippon) 126 of 171 (73.7%) microsatellite primers gave a product with 47 (37.3%) polymorphic. The proportion of bovine microsatellite loci conserved across artiodactyl species was significantly greater in this study than previously reported. Reasons for this high degree of microsatellite conservation are discussed. We suggest that a high resolution comparative map of the artiodactyls can be constructed using microsatellites.

Background Few data are available concerning the effect of human papillomavirus (HPV) infection on HIV acquisition. Methods HIV-seronegative, sexually active 18-24 year-old Kenyan men within a randomized trial of male circumcision provided penile exfoliated cells from two anatomical sites (glans/coronal sulcus, and shaft) at baseline. The GP5+/6+ PCR assay ascertained a wide range of HPV DNA types at the baseline visit. Risk of HIV infection [95% confidence interval (CI)] was estimated using Kaplan-Meier methods, and hazard ratios (HR)[95% CI] from proportional hazards models. Results Among 2,168 uncircumcised men with baseline HPV data, 1,089 (50%) were HPV DNA positive. Cumulative incidence of HIV infection by 42-months was 5.8% [95% CI 3.6, 7.9] in men with HPV-positive glans specimens versus 3.7% [1.8, 5.6] in men with HPV-negative glans specimens (p=0.01). Controlling for subsequent circumcision status, baseline HSV-2 serostatus, and sexual and sociodemographic risk factors, the HR of HIV infection in men with HPV-positive glans specimens was 1.8 [1.1, 2.9] compared to men with HPV-negative glans specimens. Conclusion Results suggest an independent, increased risk of HIV seroconversion among HPV positive men. If confirmed in other studies, HPV prevention could be another tool for HIV prevention.