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Differential Type I Interferon Induction by Respiratory Syncytial Virus and Influenza A Virus In Vivo

Nancy A. Jewell,¹ Negin Vaghefi,^1, Sara E. Mertz,¹ Parvis Akter,¹ R. Stokes Peebles Jr.,² Lauren O. Bakaletz,^1,3 Russell K. Durbin,¹ Emilio Flaño,^1,3 and Joan E. Durbin^1,3*

Columbus Children's Research Institute, Columbus, Ohio 43205,¹ Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232,² Department of Pediatrics, The Ohio State University College of Medicine, Columbus, Ohio 43210³

Received 13 March 2007/ Accepted 29 June 2007

Type I interferon (IFN) induction is an immediate response to virus infection, and very high levels of these cytokines are produced when the Toll-like receptors (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 difference affects IFN-/ß induction in vivo. In this study, we investigated type I IFN production triggered by RSV or influenza A virus infection of BALB/c mice and found that while both viruses induced IFN-/ß 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-/ß in response to either infection, but in pDC-depleted animals only type I IFN induction by influenza virus was impaired.

Published ahead of print on 11 July 2007.

Present address: Department of Obstetrics, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095.