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Journal of Virology, July 2005, p. 9351-9355, Vol. 79, No. 14
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.14.9351-9355.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Ashley Lyon,1,
Shinichiro Yada,1,
Bao Lu,2
Craig Gerard,2 and
Sally R. Sarawar1*
La Jolla Institute for Allergy and Immunology, 10355 Science Center Dr., San Diego, California 92121;,1 Department of Pediatrics, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and,2 College of Veterinary Medicine, Chonnam National University, Gwanju, South Korea3
Received 13 January 2005/ Accepted 13 April 2005
The chemokine IP-10 (CXCL10) and its cellular receptor CXCR3 are upregulated in the lung during murine gammaherpesvirus 68 (MHV-68) infection. In order to determine the role of the CXCR3 chemokine receptor in the immune response to MHV-68, CXCR3/ mice were infected with the virus. CXCR3/ mice showed delayed clearance of replicating MHV-68 from the lungs. This correlated with delayed T-cell recruitment to the lungs and reduced cytolytic activity prior to viral clearance. Splenomegaly and the numbers of latently infected cells per spleen were transiently increased. However, CXCR3/ mice showed normal virus-specific antibody titers and effective long-term control of MHV-68 infection.
Present address: Torrey Pines Institute for Molecular Studies, San Diego, Calif.
Present address: Department of Medicine and Clinical Science, Kyushu University, Fukuoka, Japan.
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