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Journal of Virology, November 2001, p. 10730-10737, Vol. 75, No. 22
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.22.10730-10737.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Involvement of Toll-Like Receptor 4 in Innate Immunity to Respiratory Syncytial Virus

Lia M. Haynes,1 Deborah D. Moore,1 Evelyn A. Kurt-Jones,2 Robert W. Finberg,2 Larry J. Anderson,1 and Ralph A. Tripp1,*

Respiratory and Enteric Virus Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333,1 and Department of Medicine, University of Massachusetts Medical Center, Worcester, Massachusetts 016052

Received 8 March 2001/Accepted 13 August 2001

The mammalian Toll-like receptor 4, TLR4, is an important component in the innate immune response to gram-negative bacterial infection. The role of TLR4 in antiviral immunity has been largely unexplored. In this study, the in vivo immune responses to respiratory syncytial virus (RSV) and influenza virus infection were examined in TLR4-deficient (C57BL/10ScNCr) and TLR4-expressing (C57BL/10Sn) mice. TLR4-deficient mice challenged with RSV, but not influenza virus, exhibited impaired natural killer (NK) cell and CD14+ cell pulmonary trafficking, deficient NK cell function, impaired interleukin-12 expression, and impaired virus clearance compared to mice expressing TLR4. These findings suggest that Toll signaling pathways have an important role in innate immunity to RSV.

* Corresponding author. Mailing address: Division of Viral and Rickettsial Diseases, Respiratory Enteric Virology Branch, National Center for Infectious Diseases, 1600 Clifton Rd. NE, Mailstop G-09, Atlanta, GA 30333. Phone: (404) 639-3427. Fax: (404) 639-1307. E-mail: rgt3{at}cdc.gov.

Journal of Virology, November 2001, p. 10730-10737, Vol. 75, No. 22
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.22.10730-10737.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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