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Journal of Virology, May 2008, p. 5109-5114, Vol. 82, No. 10
0022-538X/08/$08.00+0 doi:10.1128/JVI.00060-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Naglaa H. Shoukry,2,
Arash Grakoui,3
Michael J. Fuller,1
Andrew G. Cawthon,1
Christine Dong,4
Dana L. Hasselschwert,5
Kathleen M. Brasky,6
Gordon J. Freeman,7
Nilufer P. Seth,8
Kai W. Wucherpfennig,8
Michael Houghton,4 and
Christopher M. Walker1,9*
Center for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio,1 University of Montreal Hospital Centre (CHUM) and Department of Medicine, University of Montreal, Montreal, Quebec, Canada,2 Emory University, Atlanta, Georgia,3 New Iberia Research Center, New Iberia, Louisiana,5 Southwest Foundation for Biomedical Research, San Antonio, Texas,6 Department of Medical Oncology,7 Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts,8 Novartis Corporation, Emeryville, California,4 College of Medicine and Public Health, Ohio State University, Columbus, Ohio9
Received 9 January 2008/ Accepted 3 March 2008
The inhibitory receptor programmed death-1 (PD-1) is present on CD8+ T cells in chronic hepatitis C virus (HCV), but expression patterns in spontaneously resolving infections are incompletely characterized. Here we report that PD-1 was usually absent on memory CD8+ T cells from chimpanzees with resolved infections, but sustained low-level expression was sometimes observed in the absence of apparent virus replication. PD-1-positive memory T cells expanded and displayed antiviral activity upon reinfection with HCV, indicating conserved function. This animal model should facilitate studies of whether PD-1 differentially influences effector and memory T-cell function in resolved versus persistent human infections.
Published ahead of print on 12 March 2008.
D.G.B. and N.H.S. contributed equally to this work.
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