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The Journal of Immunology, 2007, 178: B179.
Copyright © 2007 by The American Association of Immunologists, Inc.
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B179

Differential Type I Interferon Induction by Respiratory Viruses

Joan E. Durbin1, Nancy A. Jewell1, Negin Vaghefi1, Sara E. Mertz1, Parvis Akter1, R. Stokes Peebles, Jr.2, Lauren O Bakaletz3, Russell K. Durbin1 and Emilio Flano1

1 Center for Vaccines and Immunity, Columbus Children’s Research Institute, 700 Children’s Drive, Columbus, Ohio, 43205, 2 Department of Medicine, Vanderbilt University College of Medicien, T-1217 MCN, Vanderbilt University Medical Center, Nashville, TN, 37232, 3 Center for Microbial Pathogenesis, Columbus Childrens Research Institute, 700 Children’s Drive, Columbus, Ohio, 43205

Abstract

Type I interferon (IFN) induction is an immediate response to virus infection, and very high levels of these cytokines are produced when the TLRs expressed at high levels by plasmacytoid dendritic cells (pDCs) are triggered by viral nucleic acids. Unlike many RNA viruses, respiratory syncytial virus (RSV) does not appear to activate pDCs through their TLRs, and it is not clear how this property impacts IFN-alpha/beta induction by this virus in vivo. In this study we compared type I IFN production by RSV and influenza A virus infection of BALB/c mice and found that while both viruses induced IFN-alpha/beta production by pDCs in vitro, only influenza virus infection could stimulate type I IFN synthesis by pDCs in vivo. In situ hybridization studies demonstrated that the infected respiratory epithelium was a major source of IFN-alpha/beta in response to either virus; but in pDC-depleted animals only type I IFN induction by influenza virus infection was impaired.

This work was supported by grants R01AI47226 and R01DC006468 to JED from the National Institutes of Health.





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