Distribution of human papillomaviruses and bacterial vaginosis in HIV positive women with abnormal cytology in Mombasa, Kenya

Sonia Simone Menon, Rodolfo Rossi, Ronald Harebottle, Hillary Mabeya, Davy vanden Broeck

HPV is the major etiological factor in the causal pathway for cervical cancer, which is the leading cancer among women in sub-Saharan Africa. HIV is associated with a higher prevalence and a broader range of high-risk HPV genotypes. Studies have shown a positive association between Bacterial vaginosis (BV) and HPV and HIV. Also, in African women, BV was found to be significantly associated with vaginal inflammation. The high prevalence of BV, HIV and HPV infections in the African continent makes elucidation of the interactions with one another of utmost public health interest. The aims of the current study are to examine the frequency of HPV genotypes and BV as well as their respective risk factors within an HIV infected population with abnormal cytology in the resource-constrained setting of Mombasa, Kenya and, secondly, highlight issues to consider for triple co-infection clinical management. Cross-sectional analysis with a sample drawn from an ongoing cohort study. All consenting, non-pregnant HIV infected women, between 18 and 50 years of age, without a history of cervical cancer or hysterectomy, between November 2005 and April 2006 were screened for HR HPV DNA in Mombasa, Kenya. 1 out of 4 HIV positive women fulfilled the criteria by having SIL (24.9 %). 600 HIV infected women were tested to reach a cohort of 74 HIV women with abnormal cytology. To assess which factors were associated with HR HPV, crude statistical analysis was performed through logistic regression. Bacterial vaginosis (BV) was found in 46 women out of 74 (62.2 %). Cervicitis was diagnosed in 15 % of women (n = 11), of which 8 had BV. The most prevalent HPV genotypes were HPV 16 (33.8), HPV 53 (24.3) and HPV 18 (17.6 %), while 65 % of the participants had multiple genotype infection. Statistically significant associations between CD4 counts <200 cells/μl and multiple HPV prevalence, adjusted for age were also noted (OR = 3.7; 95 CI: 1.2-12.1; p = 0.03) and HPV53 (OR = 4.4, 95 % CI: 1.4-13.6; p = 0.01). A statistically significant association was found between CD4 count ≥ 350 μl and HPV 16 adjusted for age (OR = 2.9; 95 % CI: 1.0- 8.3; p = 0.05). A borderline statistically significant association was observed between BV and HPV58 (crude OR = 4.1, 95 % CI: 0.8-21.0; p = 0.07). The most prevalent HPV genotypes observed were HPV 16, HPV 53, and HPV 18, which have a combined prevalence of 76 %. Our results show that a triage based on CD4 count should start at CD4 count ≥ 350 μl as our study suggests that HPV 16 are more prevalent when women are moderately immunosuppressed. Given the high prevalence of HPV 53 in a HIV infected population with abnormal cytology, its cervical carcinoma genesis potential as a stand-alone genotype and as well as its synergism with multiple infections should be investigated. The new WHO guideline in resource-poor settings to rescreen women for HPV within ten years may be more effective if BV and cervicitis management become a major component for HIV-HPV management.