According to the World Health Organization (WHO), invasive cervical cancer (ICC) is the second most common cancer in women worldwide and is more frequent in low-income countries [19
]. Recent guidelines recommend that, following two initial normal Pap-smears at a 6-month interval, all HIV-positive women should undergo annual cervical cytologic examination. In addition, it is recommended that all immunosuppressed women with atypical squamous cells undergo colposcopy [20
]. In our study the prevalence of precancerous lesions was 26.7% (191). In other studies among HIV-infected women in Lusaka, Zambia was 79% prevalence of high-grade squamous intraepithelial lesions (HSIL) of the cervix [21
] and the high prevalence of HPV-DNA in Zambia study (97.2% for any HPV and 90.3% for any HR-HPV) [22
]. In Guinea, overall human papillomavirus prevalence was 50.8% (78.5% and 47.9% among women with and without cervical abnormalities, resp.) [23
]. A recent meta-analysis shows that the HPV prevalence was 56.6% in Africa, 31.1% in Asia, 32.4% in Europe, 31.4% in North America, and 57.3% in South/Central America [24
]. Although the mechanism by which HIV increases risk of cervical cancer is not completely understood, studies suggest that HIV-induced immunosuppression leads to an inability to control the expression of HPV and the production of HPV oncoproteins E6 and E7 [25
] and the risk appears to be associated with increased HPV persistence that may result from immunosuppression related to HIV. Furthermore, the risk is greater in women with CD4 counts less than 200 cells per microliter and in those with high plasma HIV RNA levels [27
]. Studies have shown that HIV-1 infection is associated with an increased rate of HPV infection, mainly restricted to HR-HPV types which are the cause of invasive cancer of the cervix [28
]. Several studies conducted in sub-Saharan Africa indicate that among African women, being HIV infected was associated with a high risk of presenting squamous intraepithelial lesions of the cervix, with ORs ranging from 4.4 to 17 depending on the grade of the lesion and other factors [28
]. Yet, many case-referent studies conducted in Uganda, Rwanda, and Côte d'Ivoire failed to demonstrate any significant association between HIV and ICC, with ORs ranging from 1.1 to 1.6 [34
]. Case-referent studies in South Africa also found a significant association with ORs of 1.6 and 1.6 [38
]. In another case-referent study conducted in Kenya, HIV-positive women were also more likely to be HPV infected compared to HIV-negative women (OR = 3.1) [40
]. A cross-sectional study determined the prevalence of HPV infection, HIV infection, and cervical cytological abnormalities in Ugandan women presenting to a sexually transmitted infection clinic [41
] and found 49 cases of HPV infection among 106 women with cervical swabs adequate for HPV testing (46.2%). Similarly, a study realized in Zambia among 145 HIV-infected women of which 93.8% had abnormal Pap smears [22
]. In other study of women initiating ARV therapy recorded an exceptionally high prevalence of cervical abnormalities (66%) [42
]. This finding has implications for future interventions in the implementation of prophylactic HPV vaccines to be the part of care and support programme for HIV-infected women.
In our study those women whose current CD4 count was less than 200 were 1.6 times more likely to have precancerous cervical cancer lesions than those patients with a current CD4 count above 200. However, regarding the effect of immune function, previous studies have consistently demonstrated that the amount of CD4 cell count is a significant predictor for having or developing CIN [43
]. Given the low CD4 counts in our study population, severe immunosuppression is the most likely explanation for the high prevalence of cervical abnormalities and precancerous cervical lesions detected.
In HIV infection, lower CD4 counts have been associated with a higher prevalence of HPV infection [5
] and persistent shedding of HPV DNA [47
]. HPV viral load increases with immune suppression, likely accounting for greater facility of HPV DNA detection [46
]. In this study there was a positive association between having a CD4 count of <200. This suggests that as the CD4 count declines, vigilant followup of the anogenital tract, particularly with cervical cytological and/or histological screening, is warranted [49
In our analysis non-ART patients were 2.21 times more likely to have CIN infection than ART patients. Similar findings have been documented in other studies. As HIV-infected women continue to live longer with ART support, albeit in a moderately immunosuppressed state, they may be at increased risk for CIN and invasive cervical cancer [11
]. However, studies on the impact of HAART on the natural history of cervical squamous intraepithelial lesions have produced inconsistent results [14
]. Antiretroviral therapy (ART) for PLHIV provides a golden opportunity to increase cervical screening through the integration of ART services with frequent screening of women for cervical cancer [21
]. Starting HAART has an impact on reducing the incidence and progression and facilitating the regression of CIN infection and cervical abnormalities.
The study should be interpreted in light of the strength and limitations. Major strengths of our study include the large number of women, high participation, and reliance on cost-effective, simple, timely VILI testing. The Limitations include but not limited to the lack of information on some of the variables that can predict cervical cancer in HIV-infected women like the use of oral contraceptives or estrogens, information on sexual behavior, and smoking [49
] and the cross-sectional nature of this study allows the possibility for confounding so it is difficult to reach any causality. This may hence hinder the generalizability of our findings.