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Journal of Dental Research, Vol 76, 634-640, Copyright © 1997 by International & American Associations for Dental Research Online Journals
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N. Shine, K. Konopka and N. Duzgunes
Department of Microbiology, University of the Pacific, School of Dentistry, San Francisco, California 94115-2399, USA.
This review summarizes the data on the anti-human immunodeficiency virus (HIV) activity associated with saliva and the possible routes of oral transmission of HIV. Saliva can be passed from an HIV-infected individual to an uninfected person via sexual or non-sexual activities. The relative risk of HIV transmission through saliva is a subject of continuing concern for dental practitioners. HIV-infected individuals frequently have oral lesions that can cause bleeding and release of the virus into the oral cavity. In addition, viral p24 and HIV-1 RNA were detected in tonsils and adenoids even in asymptomatic seropositive individuals. Nevertheless, the potential HIV-infectivity of saliva is low, although both infectious HIV-1 and HIV DNA have been detected in saliva. This observation has led to the suggestion that saliva may contain factors that inhibit HIV-1 infectivity. At least two anti-HIV activities have been partially characterized: (i) physical entrapment of HIV by high-molecular-weight molecules (e.g., mucins), and (ii) inhibition of viral infection by soluble proteins. Several studies have indicated that, of the salivary proteins evaluated, recombinant secretory leukocyte protease inhibitor (rSLPI) could inhibit HIV-1 infection in macrophages at physiological concentrations. The anti-HIV activity of the serine protease inhibitor rSLPI is most likely due to its interaction with a cell-surface molecule(s) other than the primary HIV-1 receptor, CD4, and may involve (i) inhibition of cell-surface serine protease(s), and/or (ii) interaction with other human-specific co-factors essential for viral entry.
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