| First Author | Zhou S | Year | 2010 |
| Journal | J Virol | Volume | 84 |
| Issue | 18 | Pages | 9452-62 |
| PubMed ID | 20592086 | Mgi Jnum | J:307848 |
| Mgi Id | MGI:6511420 | Doi | 10.1128/JVI.00155-10 |
| Citation | Zhou S, et al. (2010) Induction and inhibition of type I interferon responses by distinct components of lymphocytic choriomeningitis virus. J Virol 84(18):9452-62 |
| abstractText | Type I interferons (IFNs) play a critical role in the host defense against viruses. Lymphocytic choriomeningitis virus (LCMV) infection induces robust type I IFN production in its natural host, the mouse. However, the mechanisms underlying the induction of type I IFNs in response to LCMV infection have not yet been clearly defined. In the present study, we demonstrate that IRF7 is required for both the early phase (day 1 postinfection) and the late phase (day 2 postinfection) of the type I IFN response to LCMV, and melanoma differentiation-associated gene 5 (MDA5)/mitochondrial antiviral signaling protein (MAVS) signaling is crucial for the late phase of the type I IFN response to LCMV. We further demonstrate that LCMV genomic RNA itself (without other LCMV components) is able to induce type I IFN responses in various cell types by activation of the RNA helicases retinoic acid-inducible gene I (RIG-I) and MDA5. We also show that expression of the LCMV nucleoprotein (NP) inhibits the type I IFN response induced by LCMV RNA and other RIG-I/MDA5 ligands. These virus-host interactions may play important roles in the pathogeneses of LCMV and other human arenavirus diseases. |
