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© 2005 The American Thoracic Society
Pathogenesis of Respiratory Syncytial Virus Infection in the Murine Model
Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee; and Vaccine Research Center, National Institute of Allergy and Infectious Diseases/National Institutes of Health, Bethesda, Maryland
Correspondence and requests for reprints should be addressed to Barney Graham, M.D., Ph.D., Vaccine Research Center, NIAID/NIH, 40 Convent Drive, Building 40, Room 2502, Bethesda, MD 20892-3017. E-mail: bgraham{at}nih.gov
There is a wide spectrum of illness caused by respiratory syncytial virus (RSV) infection that is caused in large part by host-related factors, such as age of the patient and degree of host immunocompetency. Although the vast majority of persons infected with RSV experience symptoms of mild upper respiratory tract infection, in some people these infections cause significant morbidity and are sometimes fatal. Although a great deal of investigation in both humans and animals has explained the timing and tropism of RSV infection and the general principles by which the immune system responds to this infection, at present we only partially understand the disparity in illness severity that can occur. This article briefly reviews the clinical sequelae of RSV infection and then focuses on the mechanisms of viral pathogenesis.
Key Words: airway hyperreactivity • interleukin-17 • mucus • pathology • T cells
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