Previous Article | Next Article ![]()
Journal of Virology, January 2006, p. 663-670, Vol. 80, No. 2
0022-538X/06/$08.00+0 doi:10.1128/JVI.80.2.663-670.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109,1 Program in Molecular and Cellular Biology, University of Washington, Seattle, Washington 98195,2 Oregon National Primate Research Center,3 Vaccine and Gene Therapy Institute, Oregon Health Science University, Beaverton, Oregon 970064
Received 16 September 2005/ Accepted 28 October 2005
Foamy viruses (FV) are the oldest known genus of retroviruses and have persisted in nonhuman primates for over 60 million years. FV are efficiently transmitted, leading to a lifelong nonpathogenic infection. Transmission is thought to occur through saliva, but the detailed mechanism is unknown. Interestingly, this persistent infection contrasts with the rapid cytopathicity caused by FV in vitro, suggesting a host defense against FV. To better understand the tissue specificity of FV replication and host immunologic defense against FV cytopathicity, we quantified FV in tissues of healthy rhesus macaques (RM) and those severely immunosuppressed by simian immunodeficiency virus (SIV). Contrary to earlier findings, we find that all immunocompetent animals consistently have high levels of viral RNA in oral tissues but not in other tissues examined, including the small intestine. Strikingly, abundant viral transcripts were detected in the small intestine of all of the SIV-infected RM, which has been shown to be a major site of SIV (and human immunodeficiency virus)-induced CD4+ T-cell depletion. In contrast, there was a trend to lower viral RNA levels in oropharyngeal tissues of SIV-infected animals. The expansion of FV replication to the small intestine but not to other CD4+ T-cell-depleted tissues suggests that factors other than T-cell depletion, such as dysregulation of the jejunal microenvironment after SIV infection, likely account for the expanded tissue tropism of FV replication.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»