Thursday, 2nd of August 2012 |
Abstract below and at |
C.F. Houlihan1,2, N.L. Larke1, D. Watson-Jones1,2, K.K. Smith-Mccune3,4, S. Shiboski5, P.E. Gravitt6, J.S. Smith7, L. Kuhn8,9, C. Wang10, R. Hayes1
1London School of Hygiene and Tropical Medicine, London, United Kingdom, 2Mwanza Intervention Trials Unit, Mwanza, United Republic of Tanzania, 3University of California San Francisco, Department of Obstetrics, Gynecology and Reproductive Sciences, San Francisco, United States, 4University of California San Francisco, Helen Diller Family Comprehensive Cancer Center, San Francisco, United States, 5University of California San Francisco, Department of Epidemiology and Biostatistics, San Francisco, United States, 6Johns Hopkins University, Bloomberg School of Public Health, Baltimore, United States, 7University of North Carolina - Chapel Hill, North Carolina, United States, 8Columbia Mailman School of Public Health, Department of Epidemiology, New York, United States, 9Columbia University College of Physicians & Surgeons, Sergievsky Center, New York, United States, 10University of Cape Town, Department of Pathology, Cape Town, South Africa
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Background: Human papillomavirus (HPV), one of the commonest sexually transmitted infections, may be a cofactor in HIV acquisition. We systematically reviewed the evidence for an association of HPV infection with HIV acquisition in women, heterosexual men and men who have sex with men (MSM).
Methods: Studies meeting inclusion criteria in Pubmed, Embase and conference abstracts up to 31/07/11 were identified. Random effects meta-analyses were performed to calculate summary hazard ratios (HR). Publication bias was formally tested using Begg's test and heterogeneity was assessed via the I2 statistic. A components approach was used to evaluate bias within studies.
Results: Eight papers were included, with previously unpublished data received from five authors. Seven of the eight studies found an association between HPV infection and HIV acquisition. The risk of HIV acquisition in women doubled with prevalent HPV infection with any genotype (HR=2.06 (95%CI=1.44-2.94), I2=0%, n=3). Adjustment for confounders was often inadequate and the comparison group varied between studies. The effect seen was similar for high-risk (HR=1.99 (95%CI=1.54-2.56), I2=8.4%, n=5) and low-risk (HR=2.01 (95%CI=1.27-3.20), I2=0%, n=2) HPV genotypes with weak evidence of publication bias (p=0.06). In heterosexual men and MSM, penile and anal HPV infection, respectively, were associated with HIV acquisition. However, only two studies were identified and therefore meta-analysis was not performed.
Conclusions: Meta-analysis of studies in women showed an association between prevalent HPV infection and HIV acquisition, although included studies were at risk of bias and residual confounding. A similar association was seen in MSM and heterosexual men. If further studies validate this association, HPV vaccines may reduce HIV incidence in high-HPV prevalence populations, in addition to being highly effective in the primary prevention of cervical cancer. As HPV-vaccine programs are introduced, surveillance studies will be important to monitor the impact of HPV vaccination on HIV acquisition.
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