Human papillomavirus (HPV) infection and cervical squamous intraepithelial lesions (SILs) were studied in 379 high-risk women. Human papillomavirus DNA was detected in 238 of 360 (66.1%) of the beta-globin-positive cervical samples, and 467 HPV isolates belonging to 35 types were identified. Multiple (2 -7 types) HPV infections were observed in 52.9% of HPV-infected women. The most prevalent HPV types were HPV-52 (14.7%), HPV-35 (9.4%), HPV-58 (9.4%), HPV-51 (8.6%), HPV-16 (7.8%), HPV-31 (7.5%), HPV-53 (6.7%), and HPV-18 (6.4%). Human immunodeficiency virus type 1 (HIV-1) seroprevalence was 36.0%. Human papillomavirus prevalence was significantly higher in HIV-1-infected women (87 vs 54%, prevalence ratio ( Cervical cancer is the most frequent cancer of women in developing countries, particularly in sub-Saharan Africa (Parkin et al, 1999), and it is now well established that genital infection with certain types of human papillomavirus (HPV) causes virtually all cases of cervical intraepithelial neoplasia (CIN) and invasive cervical cancer (ICC) (Walboomers et al, 1999). The HPV types that infect the genital tract have been subdivided into low-risk (LR) types, which are principally found in nonmalignant lesions such as genital warts, and high-risk (HR) types, which are associated with the development of CIN and ICC. Human papillomavirus types 6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81, and 89 are classified as LR types, whereas types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82 are classified as HR types. In addition, HPV types 26, 53, and 66 are considered as probably carcinogenic (Muñoz et al, 2003).Human papillomavirus prophylactic vaccines are now being developed and promising results have been obtained with recombinant L1 capsid protein virus-like particles (VLPs). However, the current HPV vaccines target the most prevalent high-risk HPV (HR-HPV) types worldwide, namely HPV-16 and HPV-18 (Koutsky et al, 2002;Ault et al, 2004;Brown et al, 2004;Harper et al, 2004). It has been shown that crossneutralisation induced by L1 VLPs represents less than 1% of the neutralising activity induced by the dominant conformational epitope , indicating that current HPV vaccines would be able to confer only type-specific immunity. Therefore, effectiveness of these vaccines on the prevention of cancer may be lower in populations highly affected by HR-HPV types other than HPV-16 and HPV-18. Thus, it is important to document the distribution of HPV genotypes in HPV-infected women and in women with cervical neoplasia in African countries in order to assess the potential effectiveness of a bivalent HPV-16/18 vaccine.There have been few detailed studies of HPV genotypes and their association with intraepithelial lesions or ICC in sub-Saharan Africa. Available data suggest, however, a higher prevalence and wider spectrum of oncogenic HPV types compared to studies conducted elsewhere (Castellsague et al, 2001;De Vuyst et al, 2003;Mayaud et al, 2003;Clifford et al, 2005;Wall et al, 2005). Furthermore, the high backgr...

BackgroundHuman papillomaviruses are the most common sexually transmitted infections, and genital warts, caused by HPV-6 and 11, entail considerable morbidity and cost. The natural history of genital warts in relation to HIV-1 infection has not been described in African women. We examined risk factors for genital warts in a cohort of high-risk women in Burkina Faso, in order to further describe their epidemiology.MethodsA prospective study of 765 high-risk women who were followed at 4-monthly intervals for 27 months in Burkina Faso. Logistic and Cox regression were used to identify factors associated with prevalent, incident and persistent genital warts, including HIV-1 serostatus, CD4+ count, and concurrent sexually transmitted infections. In a subset of 306 women, cervical HPV DNA was tested at enrolment.ResultsGenital wart prevalence at baseline was 1.6% (8/492) among HIV-uninfected and 7.0% (19/273) among HIV-1 seropositive women. Forty women (5.2%) experienced at least one incident GW episode. Incidence was 1.1 per 100 person-years among HIV-uninfected women, 7.4 per 100 person-years among HIV-1 seropositive women with a nadir CD4+ count >200 cells/μL and 14.6 per 100 person-years among HIV-1 seropositive women with a nadir CD4+ count ≤200 cells/μL. Incident genital warts were also associated with concurrent bacterial vaginosis, and genital ulceration. Antiretroviral therapy was not protective against incident or persistent genital warts. Detection of HPV-6 DNA and abnormal cervical cytology were strongly associated with incident genital warts.ConclusionsGenital warts occur much more frequently among HIV-1 infected women in Africa, particularly among those with low CD4+ counts. Antiretroviral therapy did not reduce the incidence or persistence of genital warts in this population.