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Sir: The contribution of 2 sexually transmitted viruses, namely human papillomavirus (HPV) and HIV, in the development of cervical neoplasia has been clearly established worldwide1. The actual role of a third sexually transmitted virus, herpes simplex type 2, remains unclear2,3. Very few studies have in fact shown an association between cervical dysplasia–neoplasia and bacterial or parasitic sexually transmitted infections (STIs)4. The interrelationship between sexual behaviour, HPV, HIV and other STIs makes it difficult to pull out ‘classical’ STIs as independent risk factors for cervical neoplasia.
Recently Takac et al.5 compared the frequency of Chlamydia trachomatis infection in women with and without cervical dysplasia, showing no association between chlamydial infection and dysplasia. They conclude that chlamydial infection seems not to interfere with the development or the promotion of cervical dysplasia. We would like to share our experience in this field from a study with both a cross-sectional and a prospective component, conducted in African women with high HIV and STI prevalences.
Between 1995 and 1996, 2037 women underwent both cervical and STI screenings in 3 outpatient gynaecology clinics in Abidjan, Côte d’Ivoire6. In this sample, the prevalence of cervical dysplasia–neoplasia was 11.8%; it was 7.8% for low-grade squamous intraepithelial lesions (SILs), 3.1% for high-grade SILs and 0.9% for invasive carcinomas (ICs). Table 1 shows that HPV and HIV were the only infections associated with cervical dysplasia–neoplasia in univariate analysis, and HPV infection played the main role; HIV-1 was associated with SILs and HIV-2 with ICs. Bacterial and parasitic STIs were not associated with SILs or ICs, even after adjustment for potential confounders as parity, age at first intercourse and number of sexual partners. Low-grade SILs were less frequent in women with candidiasis (P= 0.022), but this relation disappeared when taking into account HPV and HIV results.
Of the women with low-grade SILs, 94 were followed up to assess the short-term evolution of these lesions7. A median of 5 months after the initial smear, HIV-1 and HPV were the only infections significantly associated with the persistence of SILs in univariate analysis, and HIV-1 infection played the main role. Persistence of SILs was slightly more frequent in women with chlamydial infection at enrolment (P= 0.059), but this relation disappeared in multivariate analysis. These results reinforce the marginal contribution, if any, of classical and curable STIs in the occurrence and progression of cervical dysplasia–neoplasia5,8,9.