Abstract
Antiviral transcriptional responses and regulated cell death are crucial components of the host response to virus infection. However, in contrast to the signaling pathways that promote antiviral transcription, those that initiate cell death following virus infection are less understood. Several recent studies have identified pattern recognition receptors (PRRs) of the mammalian innate immune system that activate cell death pathways. These same receptors also have established roles in the induction of antiviral gene expression. In this review we discuss the mechanisms by which PRRs can serve dual roles as initiators of inflammatory gene expression and as inducers of apoptosis and necroptosis following virus infection.
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