Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 18, Pages 9790-9800Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00530-07
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Funding
- NIAID NIH HHS [R01 AI 47226, R01 AI047226] Funding Source: Medline
- NIDCD NIH HHS [R01 DC 006468, R01 DC006468] Funding Source: Medline
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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-alpha/beta induction in vivo. In this study, we investigated type I IFN production triggered by RSV or influenza A virus infection of BAILB/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 infection, but in pbC-depleted animals only type I IFN induction by influenza virus was impaired.
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