© 2004 by Oxford University Press
© 2004 Oxford University Press
EDITORIAL |
Cervical Neoplasia and Highly Active Antiretroviral Therapy
Affiliation of authors: Department of Pathology, School of Medicine, University of Washington, Seattle
Correspondence to: Nancy B. Kiviat, MD, Department of Pathology, University of Washington, 1914 N 34th St., Ste. 300, Seattle, WA 98103 (e-mail: nbk@u.washington.edu)
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Previous studies have clearly demonstrated that human immunodeficiency virus (HIV)-infected women, especially those with low CD4+ T-cell counts, are at increased risk for infection with human papillomaviruses (HPVs) (1,2), the etiologic agent for the development of cervical cancer. Furthermore, HIV infection has been shown to increase a woman's risk of cervical cancer and of cervical cancer precursor lesions (3), including high-, and especially, low-grade squamous intraepithelial lesions (SIL) (47). The mechanism by which HIV increases the risk of HPV infection and cervical neoplasia is believed to be related, in part, to HIV-induced immunodeficiency and the resulting inability to control HPV infection (8). Given this potential mechanism, it has been proposed that highly active antiretroviral therapy (HAART), which is known to lead to clinically significant immunologic reconstitution (9,10