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Open Access Highly Accessed Research article

HPV types, HIV and invasive cervical carcinoma risk in Kampala, Uganda: a case-control study

Michael Odida12, Sven Sandin1, Florence Mirembe3, Bernhard Kleter4, Wim Quint4 and Elisabete Weiderpass1567*

Author Affiliations

1 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77 Stockholm, Sweden

2 Department of Pathology, Faculty of Medicine, Makerere University, P.O. Box 7072, Kampala, Uganda

3 Department of Gynecology and Obstetrics, Faculty of Medicine, Makerere University, P.O. Box 7072, Kampala, Uganda

4 DDL Diagnostic Laboratory, Fonteynenburghlaan 7, 2275 CX Voorburg, the Netherlands

5 Department of Etiological Research, Cancer Registry of Norway, PB 5313 Majorstuen, 0304 Oslo, Norway

6 Department of Community Medicine, University of Tromsø, N-9037 Tromsø, Norway

7 Department of Genetic Epidemiology, Folkhälsan Research Center, Biomedicum Helsinki, PB 63, FI-00014 HU, Finland

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Infectious Agents and Cancer 2011, 6:8  doi:10.1186/1750-9378-6-8

Published: 25 June 2011

Abstract

Background

While the association of human papillomavirus (HPV) with cervical cancer is well established, the influence of HIV on the risk of this disease in sub-Saharan Africa remains unclear. To assess the risk of invasive cervical carcinoma (ICC) associated with HIV and HPV types, a hospital-based case-control study was performed between September 2004 and December 2006 in Kampala, Uganda. Incident cases of histologically-confirmed ICC (N=316) and control women (N=314), who were visitors or care-takers of ICC cases in the hospital, were recruited. Blood samples were obtained for HIV serology and CD4 count, as well as cervical samples for HPV testing. HPV DNA detection and genotyping was performed using the SPF10/DEIA/LiPA25 technique which detects all mucosal HPV types by DEIA and identifies 25 HPV genotypes by LiPA version 1. Samples that tested positive but could not be genotyped were designated HPVX. Odds ratios (OR) and 95% confidence intervals (CI) were calculated by logistic regression, adjusting for possible confounding factors.

Results

For both squamous cell carcinoma (SCC) and adenocarcinoma of the cervix, statistically significantly increased ORs were found among women infected with HPV, in particular single HPV infections, infections with HPV16-related types and high-risk HPV types, in particular HPV16, 18 and 45. For other HPV types the ORs for both SCC and adenocarcinoma were not statistically significantly elevated. HIV infection and CD4 count were not associated with SCC or adenocarcinoma risk in our study population. Among women infected with high-risk HPV types, no association between HIV and SCC emerged. However, an inverse association with adenocarcinoma was observed, while decrease in CD4 count was not associated with ICC risk.

Conclusions

The ORs for SCC and adenocarcinoma were increased in women infected with HPV, in particular single HPV infections, infections with HPV16- and 18-related types, and high-risk HPV types, specifically HPV16, 18 and 45. HIV infection and CD4 count were not associated with SCC or adenocarcinoma risk, but among women infected with high-risk HPV types there was an inverse association between HIV infection and adenocarcinoma risk. These results suggest that HIV and CD4 count may have no role in the progression of cervical cancer.