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Respiratory Syncytial Virus G Protein and G Protein CX3C Motif Adversely Affect CX3CR1⁺ T Cell Responses

Jennifer Harcourt^*, Rene Alvarez, Les P. Jones, Christine Henderson, Larry J. Anderson^* and Ralph A. Tripp^1,

^* Division of Viral and Rickettsial Diseases, Viral and Enteric Virus Branch, Centers for Disease Control and Prevention, Atlanta, GA 30333; and Center for Disease Intervention, Department of Infectious Diseases, University of Georgia, College of Veterinary Medicine, Athens, GA 30602

Interactions between fractalkine (CX3CL1) and its receptor, CX3CR1, mediate leukocyte adhesion, activation, and trafficking. The respiratory syncytial virus (RSV) G protein has a CX3C chemokine motif that can bind CX3CR1 and modify CXCL1-mediated responses. In this study, we show that expression of the RSV G protein or the G protein CX3C motif during infection is associated with reduced CX3CR1⁺ T cell trafficking to the lung, reduced frequencies of RSV-specific, MHC class I-restricted IFN--expressing cells, and lower numbers of IL-4- and CX3CL1-expressing cells. In addition, we show that CX3CR1⁺ cells constitute a major component of the cytotoxic response to RSV infection. These results suggest that G protein and the G protein CX3C motif reduce the antiviral T cell response to RSV infection.

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