In an investigation conducted in student health clinic patients, the polymerase chain reaction was used to detect human papillomavirus (HPV) DNA, thereby allowing measurement of the prevalence of HPV infection and study of the association between HPV infection and risk factors for cervical cancer. Of 159 women eligible to participate, 105 (66%) provided specimen of cervical cells for HPV typing, and also answered an interviewer‐administered questionnaire which sought information on risk factors for cervical cancer. Nucleic acid extracted from cervical cells was screened with primers for HPV types 6, 11, 16, 18, 33 and with an HPV Consensus primer. Overall, the prevalence of HPV infection was 18.1%, while for HPV‐6/11 it was 2.9% and for HPV‐16/18 it was 10.5%. There were statistically significant increases in risk of HPV infection with history of ever having smoked cigarettes (overall, and for HPV‐16 alone) and with a history of usually having sexual intercourse during menstrual periods (overall, but not for HPV‐16), and these associations were independent of the effects of age at first sexual intercourse and number of sexual partners. The latter 2 variables, as well as the total number of occasions of sexual intercourse, a history of anal intercourse, and a history of ever having used oral contraceptives, were not associated with statistically significant alterations in risk of HPV infection.

A case‐control study of 766 histologically confirmed incident cases of invasive cervical cancer and 1,532 hospital and community controls was conducted in Latin America to evaluate the etiologic role of herpes simplex virus type 2 (HSV‐2) and to examine whether HSV‐2 interacts with other risk factors. In addition to a personal interview, all subjects were asked to donate blood samples and cervical swabs for assessment of exposure to HSV‐2 and human papillomaviruses (HPVs) respectively. Ninety‐eight percent of cases and 91% of controls agreed to the interview and blood collection. Women testing positive for HSV‐2 antibodies were found to have a 60% increased risk of cervical cancer compared with seronegative women (95% CI = 1.3, 1.9). Control for education, sexual and reproductive behavior, prior Pap‐smear screening, smoking, oral contraceptive use, HPV‐6/11 DNA, or HPV‐16/18 DNA detection did not materially affect this estimate. No effect modification of HSV‐2 by age, HPV‐6/11 DNA, pregnancies, oral contraceptive use or cigarette smoking was observed. However, a significant interaction was detected between HSV‐2 and HPV‐16/18. Compared with women testing negative to both virus types, those positive for HSV‐2 alone had a RR of 1.2 (95% CI = 0.9, 1.6), those positive for HPV‐16/18 DNA alone had a RR of 4.3 (95% CI = 3.0,6.0), and those positive for both viruses had a RR of 8.8 (95% CI = 5.9, 13.0). These findings corroborate recent laboratory evidence of a possible biological interaction between HSV‐2 and HPV‐16/18 in the development of cervical cancer. Further confirmatory studies are needed, given concerns with potential misclassification of exposure by the laboratory assays utilized.

Cancer of the cervix is relatively common in China, but has been investigated epidemiologically in only a few studies. In the hospital‐based case‐control study reported here, we investigated the role of various lifestyle and dietary factors, as well as infection with human papillomavirus (HPV) types 16 and 33 and herpes simplex virus type 2 in the aetiology of invasive cervical cancer. The study was conducted in Sichuan province, and involved 101 cases with histologically‐confirmed cervical cancer recruited from the gynaecological oncology clinic of the West China University Hospital, and 146 controls recruited from patients attending the gynaecology clinic of the same hospital. Risk of cervical cancer was greatly increased in association with infection with HPV 16/33, the adjusted odds ratio for those with evidence of infection being 32.9 (95% Cl 7.7‐141.1). In contrast, infection with HSV 2 was not associated with a significantly altered risk of cervical cancer. Indices of sexual history and of dietary habits also showed no association with risk of cervical cancer, while good personal and genital hygiene were associated with markedly reduced risk. Although the results of this study are consistent with a causal role for HPV in the aetiology of cervical cancer, bias or increased viral expression following malignant transformation cannot be excluded as explanations for the strong positive association.