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RIG-I and dsRNA-induced IFNbeta activation.
Stéphane Hausmann1, Jean-Baptiste Marq, Caroline Tapparel
1Department of Microbiology and Molecular Medicine, University of Geneva Medical School, Geneva, Switzerland.
Plos One
|December 31, 2008
Summary
Most RNA viruses trigger innate immunity via RIG-I, but picornaviruses use mda-5. SeV infection, like other RNA viruses, requires RIG-I, not mda-5, for interferon induction.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Most RNA viruses initiate RNA synthesis with NTPs, leaving some viral RNAs unblocked.
- Innate immune responses to RNA viruses typically involve RIG-I, except for picornaviruses which utilize mda-5.
Purpose of the Study:
- To investigate the innate immune response triggered by Sendai virus (SeV) infection.
- To determine the role of RIG-I and mda-5 in SeV-induced interferon production.
Main Methods:
- Examined SeV infection in the context of interferon induction.
- Assessed the interaction of RIG-I with dsRNA (poly-I/C) in vitro and in vivo.
Main Results:
- SeV infection induces interferon, dependent on capped dsRNA without free 5' tri-phosphate ends.
- This SeV-induced interferon response requires RIG-I, not mda-5.
- RIG-I interacts with poly-I/C in vivo and in vitro, with poly-I/C uniquely stimulating RIG-I ATPase activity in variants lacking the C-terminal domain.
Conclusions:
- Sendai virus infection elicits an innate immune response mediated by RIG-I.
- RIG-I recognizes specific dsRNA structures, with distinct interactions observed for poly-I/C compared to other dsRNAs.
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