Nuclear-resident RIG-I senses viral replication inducing antiviral immunity

GuanQun Liu, Yao Lu, Sathya N. Thulasi Raman, Fang Xu, Qi Wu, Zhubing Li, Robert Brownlie, Qiang Liu and Yan Zhou ()
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GuanQun Liu: University of Saskatchewan
Yao Lu: University of Saskatchewan
Sathya N. Thulasi Raman: University of Saskatchewan
Fang Xu: University of Saskatchewan
Qi Wu: University of Saskatchewan
Zhubing Li: University of Saskatchewan
Robert Brownlie: University of Saskatchewan
Qiang Liu: University of Saskatchewan
Yan Zhou: University of Saskatchewan

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract The nucleus represents a cellular compartment where the discrimination of self from non-self nucleic acids is vital. While emerging evidence establishes a nuclear non-self DNA sensing paradigm, the nuclear sensing of non-self RNA, such as that from nuclear-replicating RNA viruses, remains unexplored. Here, we report the identification of nuclear-resident RIG-I actively involved in nuclear viral RNA sensing. The nuclear RIG-I, along with its cytoplasmic counterpart, senses influenza A virus (IAV) nuclear replication leading to a cooperative induction of type I interferon response. Its activation signals through the canonical signaling axis and establishes an effective antiviral state restricting IAV replication. The exclusive signaling specificity conferred by nuclear RIG-I is reinforced by its inability to sense cytoplasmic-replicating Sendai virus and appreciable sensing of hepatitis B virus pregenomic RNA in the nucleus. These results refine the RNA sensing paradigm for nuclear-replicating viruses and reveal a previously unrecognized subcellular milieu for RIG-I-like receptor sensing.

Date: 2018
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DOI: 10.1038/s41467-018-05745-w

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