Abstract
As pattern recognition receptors, cytosolic DNA sensors quickly induce an effective innate immune response. Poxvirus, a large DNA virus, is capable of evading the host antiviral innate immune response. In this review, we summarize the latest studies on how poxvirus is sensed by the host innate immune system and how poxvirus-encoded proteins antagonize DNA sensors. A comprehensive understanding of the interplay between poxvirus and DNA-sensing antiviral immune responses of the host will contribute to the development of new antiviral therapies and vaccines in the future.
Highlights
Poxvirus is a double-stranded DNA virus [1, 2] that replicates completely in the cytoplasm
We discussed the interplay between poxvirus and host antiviral innate immune factors, focusing on the stimulator of interferon genes (STING) pathway (Figure 1)
TLR9 is located in endosomes, while STING is located in the endoplasmic reticulum (ER)
Summary
Poxvirus is a double-stranded DNA (dsDNA) virus [1, 2] that replicates completely in the cytoplasm. IFI16, a member of the PYHIN protein family, recognizes the DNA virus genome in the nucleus and activates antiviral gene expression and the inflammasome-mediated immune response. The nuclear induction of IFI16 upon cell exposure to viral DNA activates the inflammasome pathway through ASC and caspase-1, resulting in the production of IL-1β and IL-18 [63] Both IFI16 and cGAS are necessary for the activation of STING, which is induced by cGAMP. Heterogeneous nuclear ribonucleoprotein A2B1 (HnRNPA2B1) recognizes viral DNA, undergoes homodimerization, and is demethylated by arginine demethylase JMJD6 at Arg226 This modification results in hnRNPA2B1 translocation to the cytoplasm and activation of the TBK1–IRF3 pathway, which enhances IFN-α/β production. Activation of RIG-I by this dsRNA induces the production of type I IFN and activation of the transcription factor NF-κB [53,54,55]
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