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HIV Infection and Human Herpesvirus-8 Oral Shedding Among Men Who Have Sex with Men

Casper, Corey MD, MPH*‡; Redman, Mary MS; Huang, Meei-Li PhD; Pauk, John MD, MPH; Lampinen, Thomas M. PhD; Hawes, Stephen E. PhD; Critchlow, Cathy W. PhD; Morrow, Rhoda Ashley PhD**; Corey, Lawrence MD*‡**; Kiviat, Nancy MD, PhD††; Wald, Anna MD, MPH*¶**

JAIDS Journal of Acquired Immune Deficiency Syndromes: March 1st, 2004 - Volume 35 - Issue 3 - p 233-238
Clinical Science

Human herpesvirus-8 (HHV-8) is frequently detected in oropharyngeal secretions from HIV-infected men who have sex with men (MSM), and contact with saliva may be an important mode of HHV-8 transmission. A total of 196 MSM were followed over 2 years to determine the correlates of HHV-8 oropharyngeal shedding. A total of 134 (68%) of 196 participants were HHV-8 seropositive upon enrollment, and 9 (15%) of 62 participants seroconverted to HHV-8 during follow-up. HHV-8 DNA was detected in 43 (22%) of 196 participants: 39 (27%) of 134 HHV-8 seropositive, 4 (8%) of 53 HHV-8 seronegative, and 5 (56%) of 9 seroconverters to HHV-8. HHV-8 was detected in 101 (15%) of 696 total oral specimens: 84 (17%) of 481 samples from HHV-8–seropositive men, 6 (3%) of 180 samples from HHV-8–seronegative men, and 11 (31%) of 35 samples from seroconverters. Using adjusted marginal structural models, HHV-8 shedding was higher in men not receiving highly active antiretroviral therapy (odds ratio 2.4, 95% CI 1.0–6.0, P = 0.06), with CD4 counts > 200 cells/mm3 (odds ratio 4.8, 95% CI 1.0–22.8, P = 0.05), or with detectable oral leukocyte esterase (odds ratio 5.0, 95% CI 2.0–12.5, P < 0.01). CD4 count, antiretroviral therapy, and oral inflammation may influence HHV-8 oropharyngeal shedding.

From the *Department of Medicine, The University of Washington, Seattle, WA; †Department of Biostatistics, The University of Washington, Seattle, WA; ¶Department of Epidemiology, The University of Washington, Seattle, WA; ††Department of Pathology, The University of Washington, Seattle, WA; **Department of Laboratory Medicine, The University of Washington, Seattle, WA; ‡Division of Infectious Disease, Fred Hutchinson Cancer Research Center, Seattle, WA; and §The Polyclinic, Seattle, WA.

Received for publication January 28, 2003; accepted November 26, 2003.

Support: NIH Grants 5R01CA055488-09, P01 AI30731 and U19 AI31448 and the Joel Meyer Infectious Disease Scholarship Grant.

Reprints: Corey Casper, University of Washington, Virology Research Clinic, 600 Broadway, Suite 400, Seattle, WA 98122 (e-mail:

© 2004 Lippincott Williams & Wilkins, Inc.