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Int J STD AIDS. 2000 January; 11(1): 67–68.
PMCID: PMC5382228
INSERM Subrepository

Sexually transmitted infections and cervical neoplasia

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.

Table 1
Risk of prevalent squamous intrapithelial lesions (SILs) and invasive carcinomas (ICs), and risk of persistence of low-grade SILs in gynaecological patients according to microbiological findings at enrolment, Abidjan: univariate analyses

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.

References

1. Mandelblatt JS, Kanetsky P, Eggert L, Gold K. Is HIV infection a cofactor for cervical squamous cell neoplasia? Cancer Epidemiol Biomark Prev. 1999;8:97–106. [PubMed]
2. Jones C. Cervical cancer: is herpes simplex virus type II a cofactor? Clin Microbiol Rev. 1995;8:549–56. [PMC free article] [PubMed]
3. Munoz N, Kato I, Bosch FX, et al. Cervical cancer and herpes simplex virus type 2: case–control studies in Spain and Colombia, with special reference to immunoglobulin-G subclasses. Int J Cancer. 1995;60:438–42. [PubMed]
4. Zhang ZF, Graham S, Yu SZ, et al. Trichomonas vaginalis and cervical cancer. A prospective study in China. Ann Epidemiol. 1995;5:325–32. [PubMed]
5. Takac I, Gorisek B. Chlamydia trachomatis infection in women with and without cervical intraepithelial neoplasia. Int J STD AIDS. 1999;10:331–3. [PubMed]
6. La Ruche G, Ramon R, Mensah-Ado I, et al. Squamous intraepithelial lesions of the cervix, invasive cervical carcinoma, and immunosuppression induced by human immunodeficiency virus in Africa. Cancer. 1998;82:2401–8. [PubMed]
7. La Ruche G, Leroy V, Mensah-Ado I, et al. Short-term follow up of cervical squamous intraepithelial lesions associated with HIV and human papillomavirus infections in Africa. Int J STD AIDS. 1999;10:363–8. [PubMed]
8. Jha PK, Beral V, Peto J, et al. Antibodies to human papillomavirus and to other genital infectious agents and invasive cervical cancer risk. Lancet. 1993;341:1116–18. [PubMed]
9. Schwebke JR, Zajackowski ME. Effect of concurrent lower genital tract infections on cervical cancer screening. Genitourin Med. 1997;73:383–6. [PMC free article] [PubMed]