© 2003 by Oxford University Press
Journal of the National Cancer Institute, Vol. 95, No. 14, 1062-1071,
July 16, 2003
© 2003 Oxford University Press
ARTICLE |
Human Papillomavirus Type 16 and Immune Status in Human Immunodeficiency Virus-Seropositive Women
Affiliations of authors: H. D. Strickler, R. S. Klein, C. Hall, M. Fazzari, A. J. Durante, R. D. Burk, Albert Einstein College of Medicine, Bronx, NY; J. M. Palefsky, University of California, San Francisco; K. V. Shah, D. D. Celentano, S. Gange, Johns Hopkins University, Baltimore, MD; K. Anastos, Lincoln Medical Center, and Albert Einstein College of Medicine, Bronx; H. Minkoff, Maimonides Medical Center, Brooklyn, NY; A. Duerr, Centers for Disease Control and Prevention, Atlanta, GA; L. S. Massad, Southern Illinois University School of Medicine, Springfield; S. Cu-Uvin, Brown University, Providence, RI; M. Bacon, Georgetown University Medical Center, Washington, DC; P. Schuman, Wayne State University, Detroit, MI; A. M. Levine, University of Southern California, Los Angeles; S. Melnick, National Cancer Institute, Bethesda, MD.
Correspondence to: Howard D. Strickler, M.D., M.P.H., Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, 1300 Morris Park Ave., Belfer #1308, Bronx, NY 10461 (e-mail: Strickle{at}aecom.yu.edu).
Background: Human papillomavirus (HPV) type 16 is etiologically associated with approximately half of all cervical cancers. It is important, therefore, to determine the characteristics that distinguish HPV16 from other HPV types. A preliminary result based on cross-sectional baseline data in the Women’s Interagency Human Immunodeficiency Virus (HIV) Study (WIHS) suggested that the prevalence of HPV16 might have a weaker association with immune status in HIV-seropositive women than that of other HPV types. To address this issue, we examined HPV test results from repeated study visits in the WIHS and from an independent study, the HIV Epidemiology Research Study (HERS). Methods: HIV-seropositive women in the WIHS (n = 2058) and in the HERS (n = 871) were assessed semiannually. HPV DNA was detected in cervicovaginal lavage specimens by using polymerase chain reaction assays. Prevalence ratios were used to compare the prevalence of each HPV type in women with the lowest CD4+ T-cell counts (<200 T cells/mm3) with that of women with the highest CD4+ T-cell counts (
500 T cells/mm3). A summary prevalence ratio for each HPV type (i.e., across visits and studies) was estimated using generalized estimating equations. The association of CD4+ T-cell stratum with type-specific HPV incidence was measured using multivariable Cox regression models. All statistical tests were two-sided. Results: The prevalence ratio for HPV16 was low compared with that of other HPV types at every study visit in both cohorts. The generalized estimating equation summary prevalence ratio for HPV16 (1.25, 95% confidence interval [CI] = 0.97 to 1.62) was the smallest measured, and it was statistically significantly lower than that of all other HPV types combined (P = .01). The association of CD4+ T-cell stratum with HPV16 incidence was also among the smallest measured (hazard ratio = 1.69, 95% CI = 1.01 to 2.81). Conclusions: The prevalent and incident detection of HPV16 is more weakly associated with immune status in HIV-seropositive women than that of other HPV types, suggesting that HPV16 may be better at avoiding the effects of immune surveillance, which could contribute to HPV16’s strong association with cervical cancer.
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