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J. Virol. doi:10.1128/JVI.02402-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

SIVagm Dynamics in African Green Monkeys

Divisions of Comparative Pathology, Microbiology, and Veterinary Medicine Tulane National Primate Research Center, Covington Louisiana 70433, USA; Department of Pathology, School of Medicine, Tulane University, New Orleans, Louisiana 70112, USA; Theoretical Biology and Biophysics, Los Alamos National Laboratory, Los Alamos, NM 87545, USA; Department of Pathology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19107, USA; Gilead Sciences, Inc, Foster City, California 94404, USA; Department of Tropical Medicine, School of Public Health, Tulane University, New Orleans, Louisiana 70112, USA

^* To whom correspondence should be addressed. Email: ipandrea{at}tulane.edu.

	Abstract

The mechanisms underlying the lack of disease progression in natural SIV hosts are still poorly understood. To test the hypothesis that SIV-infected AGMs avoid AIDS due to virus replication occurring in long-lived infected cells, we infected six animals with SIVagm and treated them with potent antiretroviral therapy [ART: (PMPA, tenofovir) and (FTC, emtricitabine)]. All AGMs showed a rapid decay of plasma viremia that became undetectable 36 hours after ART initiation. Significant decrease of viral load was observed in PBMCs and intestine. Mathematical modeling of viremia decay post-ART indicates a half-life of productively infected cells ranging from 4 to 9.5 h, i.e., faster than previously reported for HIV and SIV. ART induced a slight but significant increase in peripheral CD4⁺ T-cell counts but no significant changes in CD4⁺ T-cell levels in LNs and intestine. Similarly, ART did not significantly change the levels of cell proliferation, activation and apoptosis, already low in chronically SIVagm-infected AGMs. Collectively, these results indicate that, in SIVagm-infected AGMs, the bulk of virus replication is sustained by short-lived cells; therefore, differences in disease outcome between SIVmac infection of macaques and SIVagm infection of AGMs are unlikely due to intrinsic differences of the in vivo cytopathicity between the two viruses.

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