© 1991 by Oxford University Press
Journal of the National Cancer Institute, Vol. 83, No. 14, 997-1003,
July 17, 1991
© 1991 Oxford University Press
ARTICLES
Determinants of Genital Human Papillomavirus Infection in Young Women
1(Epidemiology Program), University of California Berkeley
2(University Health Service), University of California Berkeley
3Department of Infectious Diseases, Cetus Corporation Emeryville, Calif.
4Environmental Epidemiology Branch, Division of Cancer Etiology, National Cancer Institute Bethesda, Md.
*Correspondence to: M. Michele Manos, Ph.D., Department of Infectious Diseases, Cetus Corporation, 1400 Fifty-third St., Emeryville, CA 94608
Carcinoma of the cervix has several well–established epidemiologic risk factors, including multiple sexual partners and early age at first intercourse. Human papillomavirus (HPV) infection appears to have an etiologic role in the development of cervical neoplasia, but evidence linking HPV infection to known risk factors for cervical cancer has been inconsistent. The lack of expected correlations may be due to the inaccuracy of HPV assays previously used. A polymerase chain reaction DNA amplification method for the detection of HPV was used to investigate the determinants of genital HPV infection in a cross-sectional sample of 467 women attending a university health service. In contrast to studies using less accurate detection methods, the risk factors for HPV infection found here were consistent with those for cervical neoplasia. The risk of HPV infection was strongly and independently associated with increasing numbers of sexual partners in a lifetime, use of oral contraceptives, younger age, and black race. Age at first intercourse, smoking, and history of a prior sexually transmitted disease were correlated with, but not independently predictive of, HPV infection. These results demonstrate that the key risk factors for cervical carcinoma are strongly associated with genital HPV infection. This correlation suggests that HPV has an etiologic role in cervical neoplasia and reaffirms the sexual route of HPV transmission. [J Natl Cancer Inst 83: 997–1003, 1991]
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