Author: Baum, Alina; García-Sastre, Adolfo
Title: Induction of type I interferon by RNA viruses: cellular receptors and their substrates Document date: 2009_11_1
ID: 4c1nuv2p_27
Snippet: Initially identified by Yoneyama et al. (2004) through a cDNA library screen for its ability to induce an IRF reporter upon poly(I:C) treatment, RIG-I has proven to be a key sensor of RNA virus infections and activator of the signaling cascade leading to production of type I IFN. Through a number of studies, RIG-I has been demonstrated to be the main recognition receptor for multiple RNA viruses including Newcastle disease virus (NDV), vesicular .....
Document: Initially identified by Yoneyama et al. (2004) through a cDNA library screen for its ability to induce an IRF reporter upon poly(I:C) treatment, RIG-I has proven to be a key sensor of RNA virus infections and activator of the signaling cascade leading to production of type I IFN. Through a number of studies, RIG-I has been demonstrated to be the main recognition receptor for multiple RNA viruses including Newcastle disease virus (NDV), vesicular stomatitis virus (VSV), Sendai Virus, HCV, Japanese encephalitis virus (JEV), influenza A virus, rabies virus, measles virus, and respiratory syncytial virus (RSV) Hornung et al. 2006; Kato et al. 2005 Kato et al. , 2006 Liu et al. 2007; Melchjorsen et al. 2005; Pichlmair et al. 2006; Rothenfusser et al. 2005) . The physiological importance of RIG-I is highlighted by ex vivo studies from RIG-I knockout MEFs which show drastically reduced interferon levels in response to NDV, VSV, SeV, and influenza DNS1 virus infections . Infection of RIG-I -/-mice confirm these findings, as levels of IFN and survival of the mice are greatly reduced upon infection with JEV and VSV .
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