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Type I interferons are a major and essential component of the mammalian antiviral response. While many cell types produce type I interferons following viral infection, how cells detect the virus has remained a mystery for many years. Recently, multiple genome-encoded viral recognition receptors have been identified. Interestingly, all of the major viral recognition pathways characterized thus far require TRAF3 to initiate type I interferon production. In this review, we comment on the mechanistic and biological implications for the new role of TRAF3 in innate antiviral immunity.
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Saha et al. (2006) studied this question.
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