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Journal of Virology, November 2005, p. 13759-13768, Vol. 79, No. 21
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13759-13768.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Denise S. Rodrigues,2,
,
Danielle J. Harvey,3
Christian M. Leutenegger,4 and
Ursula Esser2*
Immunology Graduate Program, University of CaliforniaDavis, Davis, California 95616,1 Department of Pathology and Laboratory Medicine, University of CaliforniaDavis, School of Medicine, Sacramento, California 95817,2 Department of Public Health Sciences, University of CaliforniaDavis, Davis, California 95616,3 Lucy Whittier Molecular and Diagnostic Core Facility, University of CaliforniaDavis, California 956164
Received 11 November 2004/ Accepted 4 August 2005
To define the possible impact of T-lymphocyte trafficking parameters on simian immunodeficiency virus (SIV) pathogenesis, we examined migratory profiles of carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled T lymphocytes in acutely SIVmac251-infected and uninfected macaques within 48 h after autologous transfer. Despite significant upregulation of homeostatic chemokine CCL19/macrophage inflammatory protein 3ß and proinflammatory chemokine CXCL9/monokine induced by gamma interferon in secondary lymphoid tissue in SIV infection, no differences in CFSE+ T-lymphocyte frequencies or cell compartmentalization in lymph nodes were identified between animal groups. By contrast, a higher frequency of CFSE+ T lymphocytes in the small intestine was detected in acute SIV infection. This result correlated with increased numbers of gut CD4 T lymphocytes expressing chemokine receptors CCR9, CCR7, and CXCR3 and high levels of their respective chemokine ligands in the small intestine. The changes in trafficking parameters in SIV-infected macaques occurred concomitantly with acute gut CD4 T-lymphocyte depletion. Here, we present the first in vivo T-lymphocyte trafficking study in SIV infection and a novel approach to delineate T-lymphocyte recruitment into tissues in the nonhuman primate animal model for AIDS. Such studies are likely to provide unique insights into T-lymphocyte sequestration in distinct tissue compartments and possible mechanisms of CD4 T-lymphocyte depletion and immune dysfunction in simian AIDS.
Contributed equally to this work.
Present address: Division of Infectious Diseases, Universidade Federal de Sao Paulo, 04039-032 Sao Paulo, Brazil.
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