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_14_1
Snippet: inflammation (Wang et al. 2004 ). However, another more recent study found the opposite effect, with TLR3 knockout mice being more susceptible to WNV infection and having higher viral load in the brain, although IFN levels in these mice were not diminished (Daffis et al. 2008) . Influenza A infections in TLR3 deficient mice also resulted in a less pathogenic phenotype despite a higher virus load in the lungs of the animals (Le Goffic et al. 2006).....
Document: inflammation (Wang et al. 2004 ). However, another more recent study found the opposite effect, with TLR3 knockout mice being more susceptible to WNV infection and having higher viral load in the brain, although IFN levels in these mice were not diminished (Daffis et al. 2008) . Influenza A infections in TLR3 deficient mice also resulted in a less pathogenic phenotype despite a higher virus load in the lungs of the animals (Le Goffic et al. 2006) . Therefore, while it appears that IFN production in animals does not require TLR3 signaling, most likely because of a functional RLR system, it is clear that this receptor does play a role in the innate and adaptive immune responses. As such, people lacking in TLR3 have been shown to be more susceptible to HSV-1 associated encephalitis ).
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