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Cytokines and Respiratory Syncytial Virus Infection

Department of Infectious Diseases, University of Georgia, College of Veterinary Medicine, Athens, Georgia

Correspondence and requests for reprints should be addressed to Ralph A. Tripp, College of Veterinary Medicine, Department of Infectious Diseases, University of Georgia, Athens, GA 30602. E-mail: ratripp{at}uga.edu

Respiratory syncytial virus (RSV) is a single-stranded negative sense RNA virus in the Paramyxovirus family that is a major cause of morbidity and life-threatening lower respiratory tract disease in infants and young children worldwide. RSV is recognized as a ubiquitous virus having considerable worldwide disease burden. Studies investigating the immune response and disease pathogenesis associated with infection attribute the interplay of the virus with host factors, particularly cytokines and chemokines, in inflammation, disease, and immune effector processes. There is convincing evidence that Th1- and Th2-type cytokine patterns determine the type of immune response to RSV infection, and that the spectrum of cytokine expression affects control mechanisms involved in the regulation of disease pathogenesis and chronicity. Thus, there is a critical need to identify virus and host mechanisms that regulate cytokine expression to allow for intervention strategies to control disease pathogenesis. In this report, we discuss the role of cytokines and chemokines in the response to RSV infection, and the potential role for suppressor of cytokine signaling (SOCS) proteins in regulating these responses.

Key Words: chemokine • cytokine • protein, suppressor of cytokine signaling • virus, respiratory syncytial

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