HIV infection increases the risk of new HPV detection and decreases the rate of HPV clearance in both women and men.

This study examined the concordance of genital human papillomavirus (HPV) infection in 254 heterosexually active couples and the impact of HIV coinfection. Genital HPV detection was significantly more common among HIV-infected women than among HIV-seronegative women (99 [68%] of 145 women vs. 33 [31%] of 107 women; P < .001); similarly, HPV detection was significantly more common among HIV-infected men than among HIV-seronegative men (67 [72%] of 93 and 65 [43%] of 150 men, respectively; P < .001). HIV-seronegative male partners of HIV-infected women had a significantly greater prevalence of HPV infection than did HIV-seronegative male partners of HIV-seronegative women (38 [58%] of 65 men vs. 27 [32%] of 85 men; P = .001), indicating that HIV coinfection in one partner has a significant impact on the prevalence of HPV genital infection in the other partner. HPV concordance between couples was associated with HIV infection status (P < .001, by Pearson's chi2 test) and was significantly higher among HIV-infected couples than among HIV-seronegative couples. Type-specific sharing of HPV was associated with HIV concordance status (P = .024). HIV-seronegative couples were more likely to share 1 HPV type and were unlikely to share >1 type, whereas HIV-infected or HIV-discordant couples were more likely to share >1 HPV type. Women with a high HPV load frequently shared HPV types with their male partners, suggesting that a high HPV load may play a role in HPV transmission between partners. In conclusion, HIV coinfection in one or both sexually active partners increased HPV prevalence and HPV type-specific concordance.

Background. Mounting evidence suggests an association between human papillomavirus (HPV) and HIV acquisition. This study aimed to explore this association among South African female sex workers (FSWs). Methods. We used data from 88 HIV-negative FSWs who participated in a vaginal gel (COL-1492) trial. Cervicovaginal rinse samples, obtained before HIV-seroconversion, were genotyped into high-risk (HR-) and low-risk (LR-) HPV. HIV-adjusted hazard ratios (aHRs) and 95% confidence intervals (CI) were estimated using Cox survival analysis. Results. HR- and LR-HPV prevalences were 70.5% (95% CI : 60.5–79.2) and 60.2% (95% CI : 49.9–70.0), respectively. Twenty-five women HIV seroconverted. Controlling for background characteristics and other sexually transmitted infections, HIV aHR increased by a factor of 1.7 (95% CI : 1.01–2.7, P linear trend = 0.045) for an increase of one unit of the number of HR-HPV genotypes. Conclusions. HIV seroconversion among FSWs is associated with genital HR-HPV infection. Further investigation is warranted, including testing the possible protective effect of available HPV vaccines on HIV acquisition.

The prevalence of HR-HPV infection was lower in compliant Carraguard users than compliant placebo users. To our knowledge, this is the first report showing a negative association of HPV infection with a vaginal microbicide.

This study tested cervical and oral human papillomavirus (HPV) infection in HIV-1 seropositive (HIV+) and seronegative (HIV-) women to determine any association between infections at both sites and the difference in prevalence of the HPV types infecting these women. Participants were 115 women referred to a colposcopy clinic after diagnosis of abnormal cervical cytology. The women showed low grade cervical intraepithelial neoplasia (CIN1) or high grade disease (CIN2/3) or no CIN based on colposcopy and histology. Typing of HPV in cervical and oral cells was by Roche linear array and included direct sequencing on selected oral samples. Cervical HPV prevalence was 86.5% and 97.1% in HIV- and HIV+ women respectively. With the exception of HPV-45, prominent in HIV+ women, the hierarchy of predominant types were similar in HIV- and HIV+ women. HPV-16 was most prevalent in both HIV+ (41.7%) and HIV- women (38.5%) with CIN2/3. Significantly more HIV+ women had multiple cervical (>1) infections than HIV- women (36.1% vs. 88.2%, P < 0.001) and more oral HPV infections (45.5% and 25% respectively; P = 0.04). The most prevalent oral HPV types were HPV-33, -11, and -72. The majority of women did not have concordant oral and cervical HPV types, reflecting possible independence of infection at the two sites. HIV immune suppression did not impact significantly on the predominant types of cervical HPV infection (except for HPV-45). HIV+ women had more multiple HPV infections and those with severe cervical disease a similar prevalence of HIV-16 but a lower HPV-18 prevalence than HIV- women.