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pubmed-article:16424189pubmed:abstractTextInteractions 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-gamma-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.lld:pubmed
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pubmed-article:16424189pubmed:articleTitleRespiratory syncytial virus G protein and G protein CX3C motif adversely affect CX3CR1+ T cell responses.lld:pubmed
pubmed-article:16424189pubmed:affiliationDivision of Viral and Rickettsial Diseases, Viral and Enteric Virus Branch, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA.lld:pubmed
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