BackgroundHigh-risk (HR) HPV genotypes other than 16 and 18 have been detected in a significant proportion of immunocompromised females. We aim to evaluate the frequency of HR HPV genotypes in a population of HIV-positive Caribbean women.MethodsOne hundred sixty-seven consecutive, non-pregnant, HIV-positive females ≥18 years were recruited in this study. Each participant received a vaginal examination, PAP smear, and completed a questionnaire. DNA was extracted for HPV testing in 86 patients.ResultsMean age was 39.1 years for women positive for HR HPV and 43.1 years for women negative for HR HPV (P value  = 0.040). 78% (130/167) of the women had HR HPV infections; the prevalence of abnormal cervical cytology was 38% among women who were HR HPV-positive compared to women who were HR HPV-negative (22%). Fifty-one percent of the 86 women with available genotype carried infections with HPV 16 and/or HPV 18; genotypes of unknown risk were also frequently observed. Women who had a CD4+ count of ≤200 had 7 times increased odds of carrying HR HPV infection in comparison to women with CD4+>200.ConclusionsHR HPV infections in HIV infected females may consist of more than just HPV 16 and 18, but also HPV 52 and 58. Further studies are needed to determine whether HPV 52 and 58 play a significant role in the development of cervical cytological abnormalities in HIV+ women.

Introduction: The human papillomavirus (HPV) is the major etiologic agent in the development of cervical cancer and its natural history of infection is altered in persons infected with the human immunodeficiency virus (HIV). The prevalence of HPV infection and cervical dysplasia in the HIV sero-positive females in the Bahamas is not known. Finding out the prevalence would allow for the establishment of protocols to optimize total care of this population and help prevent morbidity and mortality related to cervical cancer.

Background: It has been demonstrated in immunocompromised females that HR HPV genotypes other than 16 and 18 have been detected in a significant proportion of these individuals. We aim to evaluate the frequency of HR HPV genotypes in a population of HIV-positive Caribbean women, detect characteristics associated with HR HPV infections other than HPV16 and 18, and investigate the clustering of HPV genotypes in this population. Methods: One hundred and seventy-six non-pregnant, HIV-positive females ≥18 years were recruited. Each participant received a vaginal examination and completed a questionnaire. Results: Mean age was 38.7 years for women positive for HR HPV and 44.4 years for women negative for HR HPV (P value = 0.0018). The majority of the HR HPV-positive women were on HAART for 2-4 years. Non-negative matrix factorization identified HPV 16, 18, 52 and 58 as the most influential HPV high-risk types. Among the women who were HIV+ for more than 2 years, secondary CART analysis revealed those aged ≤29 had statistically significant different cervical abnormality profile compared to women >29 years; specifically, younger women were more likely to have dysplasia, while older women had normal cervical cytology. Also, the mean number of years on HAART for ≤29 years old was only 1 year (std dev. ±1.3) while those >29 years old the mean was 3.6 years (std. dev. ± 2.5) (p = 0.009). Conclusions: HR HPV in the immunocompromised female consists of more than just HPV 16 and 18, but also types HPV 52 and 58, which are likely to influence the course of HPV infections and the development of cervical cytological abnormalities. Targeted interventions to boost treatment compliance among HIV- positive women are needed to reduce the risk of cervical abnormalities. Citation Format: Elizabeth Blackman, Dionne N. Dames, Raleigh Butler, Emanuela Taioli, Stacy Eckstein, Karthik Devarajan, Andrea Griffith-Bowe, Perry Gomez, Camille Ragin. High-risk cervical human papillomavirus infections among human immunodeficiency virus-positive women in the Bahamas. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-14. doi:10.1158/1538-7445.AM2013-LB-14