Effects of Bacterial Vaginosis and Other Genital Infections on the Natural History of Human Papillomavirus Infection in HIV‐1–Infected and High‐Risk HIV‐1–Uninfected Women
1National Institute of Child Health and Human Development, Bethesda, and 2Johns Hopkins University, Baltimore, Maryland; 3Maimonides Medical Center, Brooklyn, 4Albert Einstein College of Medicine, Bronx, and 5Weill Medical College of Cornell University, New York, New York; 6University of Pittsburgh, Pittsburgh, Pennsylvania; 7Rush Presbyterian/St. Luke’s Medical Center, Chicago, Illinois; 8University of California, San Francisco, and 9University of Southern California, Los Angeles; 10Georgetown University, Washington, DC
Background.
Whether the natural history of human papillomavirus (HPV) infection is affected by bacterial vaginosis (BV) or Trichomonas vaginalis (TV) infection has not been adequately investigated in prospective studies.
Methods.Human immunodeficiency virus 1 (HIV‐1)–infected (
) and high‐risk HIV‐1–uninfected (
) women were assessed semiannually for BV (by Nugent's criteria), TV infection (by wet mount), type‐specific HPV (by polymerase chain reaction with MY09/MY11/HMB01 HPV primers), and squamous intraepithelial lesions (SIL) (by cytological examination). Sexual history was obtained from patient report at each visit. Risk factors for prevalent and incident HPV infection and SIL were evaluated by use of multivariate models.
Results.BV was associated with both prevalent and incident HPV infection but not with duration of HPV infection or incidence of SIL. TV infection was associated with incident HPV infection and with decreased duration and lower prevalence of HPV infection. TV infection had no association with development of SIL. Effects of BV and TV infection were similar in HIV‐1–infected and high‐risk HIV‐1–uninfected women. HIV‐1 infection and low CD4+ lymphocyte count were strongly associated with HPV infection and development of SIL.
Conclusions.BV and TV infection may increase the risk of acquisition (or reactivation) of HPV infection, as is consistent with hypotheses that the local cervicovaginal milieu plays a role in susceptibility to HPV infection. The finding that BV did not affect persistence of HPV infection and that TV infection may shorten the duration of HPV infection helps explain the lack of effect that BV and TV infection have on development of SIL.
Received 20 January 2004; accepted 21 September 2004; electronically published 21 February 2005.
Cited by
Online publication date: 15-May-2009.
Online publication date: 1-Feb-2009.
CrossRef
Online publication date: 1-Dec-2008.
CrossRef
Online publication date: 1-Nov-2008.
CrossRef
Online publication date: 1-Oct-2008.
CrossRef
Online publication date: 1-Dec-2007.
CrossRef
Online publication date: 25-Nov-2007.
CrossRef
Online publication date: 15-Jul-2007.
Online publication date: 1-Jun-2006.
CrossRef
Online publication date: 15-Oct-2005.
-
Presented in part: 20th International Papillomavirus Conference, Paris, 4–9 October 2002 (poster P124).
Financial support: The Women’s Interagency HIV Study is funded by the National Institute of Allergy and Infectious Diseases (grants U01‐AI‐35004, U01‐AI‐31834, U01‐AI‐34994, U01‐AI‐34989, U01‐AI‐34993, U01‐AI‐42590, and N01‐AI‐35161), the National Cancer Institute (grant NCI R01 CA85178‐01), the National Institute of Child Health and Human Development (grant U01‐HD‐32632), the National Center for Research Resources (grant MO1 RR00079), the National Institute on Drug Abuse, the National Institute of Dental Research, the Agency for Health Care Policy and Research, and the Centers for Disease Control and Prevention.