Human papillomavirus type-specific risk of cervical cancer in a population with high human immunodeficiency virus prevalence: case-control study

Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden.
Journal of General Virology (Impact Factor: 3.53). 09/2011; 92(Pt 12):2784-91. DOI: 10.1099/vir.0.034298-0
Source: PubMed

ABSTRACT There are limited data on human papillomavirus (HPV) type-specific cervical cancer risk among human immunodeficiency virus (HIV)-positive women. Previous studies have suggested that HPV 16 would be relatively less important as a causative agent among HIV-positive compared with HIV-negative women. This study investigates HPV type-specific cervical cancer risk in a population in which HIV is endemic. At the Central Hospital, Maputo, Mozambique, 221 cervical cancer cases and 203 hospital-based controls were consecutively enrolled. HPV typing from cervical samples, HIV testing and recording of socio-demographic factors were performed. Logistic regression modelling was used to assess HPV type-specific risk and effect modification between HIV and HPV infection. Infection with HPV 16, 18 and 'high-risk non-HPV 16/18 types' (HPV 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59) was associated with cervical cancer in both crude and adjusted analyses. HPV 16 and 18 were the most common types detected in cancer biopsies among both HIV-negative and HIV-positive women. There was no significant evidence of effect modification between any HPV type and HIV infection, and there were no significant differences in the HPV type-specific prevalence when cervical cancers among HIV-positive and HIV-negative women were compared. Within the limitations of the study, the relative importance of different HPV types in cervical carcinogenesis appears not to be modified greatly by HIV infection, suggesting that HPV vaccines might not need to be type-specifically modified to be suitable for populations where HIV is endemic.

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    • "Nonetheless, causal mutations of CCACs have yet to be identified. Unlike squamous cell carcinomas and non-clear cell adenocarcinomas of the cervix (Naucler et al., 2011), CCACs appear to have minimal or no association with the infection of high-risk types of the human papillomavirus (HPV) (Pirog et al., 2000; Goto et al., 2005; Stewart et al., 2006; Liebrich et al., 2009; Waggoner et al., 1994). Loss of function mutations in PTEN (phosphatase and tensin homolog deleted on chromosome 10) have been detected in HPV-negative endometrioid (2/5) and mucinous (2/6) cervical adenocarcinomas (Minaguchi et al., 2004; Hashiguchi et al., 2006) as well as CCACs of the ovary (15/40 and 6/22) (Sato et al., 2000). "
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