Résumé :
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[BDSP. Notice produite par INIST-CNRS RR0x5uj4. Diffusion soumise ... autorisation]. Human papillomaviruses (HPVs) play the major role in cervical carcinogenesis. The authors reevaluated the role of herpes simplex virus type 2 (HSV-2) in this multistage process by conducting a longitudinal, nested case-control study using 1974-1993 data and comparing the results with those from a meta-analysis of studies. A Nordic cohort of 550,000 women was followed up for an average of 5 years, after which 178 cervical carcinoma cases and 527 controls were identified. HSV-2 ; HPV-16, HPV-18, and HPV-33 ; and Chlamydia trachomatis antibodies were determined at baseline by HSV-2 glycoprotein gG-2 and HPV virus-like-particle enzyme immunoassays and by using the microimmunofluorescence method. The relative risk of cervical carcinoma was calculated by conditional logistic regression. Longitudinal studies on HSV-2 and cervical neoplasia were identified through MEDLINE (National Library of Medicine, Bethesda, Maryland), and weighted mean relative risks were calculated. Smoking (relative risk=1.6,95% confidence interval (Cl) : 1.1,2.3) and HPV-16/HPV-18/HPV-33 (relative risk=2.9,95% Cl : 1.9,4.3) were both associated with cervical carcinoma. The smoking-and HPV-16/HPV-18/HPV-33-adjusted relative risks for HSV-2 were 1.0 (95% Cl : 0.6,1.7) and 0.7 (95% Cl : 0.3,1.6), respectively, for HPV seropositives. In the meta-analysis, the relative risk for HSV-2 was 0.9 (95% Cl : 0.6,1.3). In both sets of data, HSV-2 did not play a role in cervical carcinogenesis.
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