In sub-Saharan Africa, age-standardized incidence of cervical cancer is high, ranging from 29.3 (West Africa) to 42.7 (southern Africa) per 100,000 women . The development of cervical cancer is the result of interaction of systemic and local cofactors that facilitate malignant transformation of cervical cells, with HPV infection as a necessary factor . Based on strength of association with cervical cancer, genital HPVs have been categorized by risk of acting as carcinogens in the development of cervical cancers. High-risk or oncogenic types include HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68, 73 and 82; low-risk types include HPV types 6, 11, 42, 43, 44, 54, 61, 70, 72, 81 . Examples of factors other than HPV that have been suggested as potential modulators of cervical cancer development include age and parity [4, 5], cigarette smoking , long-term oral contraceptive use , and host genetics and immunological factors .
The incidence of cervical cancer has been changing at a global level, with increasing incidence in women below 40 years of age [9, 10]. This may reflect age-cohort effects and the emergence of more aggressive histologies with a shorter natural history, possibly the result of HPV infection acquired at a younger age or of increased screening/awareness resulting in earlier detection of cervical cancer.
In HIV-infected women, there is an increased risk of HPV infection and squamous intraepithelial lesions (SIL), the precursor of cervical cancer [11, 12]. Since 1993, the revised CDC AIDS case definition has included the development of cervical cancer in an HIV-infected person as a sufficient criterion for AIDS, even in the absence of an opportunistic infection . Numerous studies have analyzed the association of HIV infection and cervical cancer [14–16]. Although positive associations between HIV infection and cervical cancer have been demonstrated [15–18], studies evaluating the strength of this association among African women have had differing conclusions [14–16, 18, 19]. It has been proposed that lack of excess risk of invasive cervical cancer among HIV-infected women in some populations may reflect the competing risk of mortality from other conditions associated with HIV infection .
Studies of HIV infection and invasive cervical cancer to date have tended to be limited by lack of information on presence of HPV DNA in cervical samples of study participants, and focused on quantifying the effect of HIV infection relative to other cofactors in the presence of HPV infection. We conducted a case-control study in a West African population to assess the relationship between cervical cancer and HIV infection, taking into account the presence of high-risk HPV infection and other cofactors such as age, parity, and lifetime number of sexual partners. In Côte d'Ivoire, the study setting, the annual incidence of cervical cancer was approximately 24.2 per 100,000  during the study period, and the prevalence of HIV infection among pregnant women attending antenatal clinics, an approximation of the prevalence in the general population, was 10% .