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Effects of Human Papillomavirus-Associated Cells on Human Immunodeficiency Virus Gene Expression

From the Departments of Obstetrics and Gynecology and Microbiology, Immunology and Molecular Genetics, UCLA School of Medicine, Los Angeles, California; Evandro Chagas Hospital Research Center, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Dipartimento di Ginecologia, Universita di Genova, Genoa, Italy; Institute of Molecular and Cellular Biology, Osaka University, Osaka, Japan; and Division of Gynecologic Oncology, Johns Hopkins University, Baltimore, Maryland.

Address reprint requests to: Otoniel Martínez-Maza, PhD, Department of Microbiology, Immunology, & Molecular Genetics, University of California Los Angeles, School of Medicine, Los Angeles, CA 90095-1747, E-mail: omartinez{at}mednet.ucla.edu

Objective: To examine the effects of soluble factors secreted by human papillomavirus (HPV)-associated cells on human immunodeficiency virus (HIV) expression.

Methods: Supernatants collected from cultured cervical biopsies and cervical cancer cell lines, and HPV-immortalized and normal keratinocytes were tested for the ability to induce HIV p24 production in two cell lines that contained latent HIV (the U1 monocytic line and the ACH-2 T cell line). Levels of HIV p24 were measured by enzyme-linked immunosorbent assay (ELISA). Culture supernatants were also assayed for the inflammatory cytokines interleukin 6, tumor necrosis factor, and interleukin 1ß by ELISA.

Results: Supernatants from all epithelial cells tested upregulated HIV p24 expression in the U1 line but not in the ACH-2 cells. Only differentiated normal keratinocytes induced p24 production by ACH-2 cells. Neutralization of the cytokines, particularly interleukin 6, partially reduced the level of HIV-inducing activity in the culture supernatants. Additionally, cervical biopsies from HIV-infected women cultured in vitro also were able to induce HIV in U1 cells but not ACH-2 cells.

Conclusions: Our results suggest that HPV infection of the cervix might influence HIV pathogenesis by inducing the production of immune and inflammatory factors that enhance HIV expression.

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