tetano
Editor, Senior Moderator
Nat Commun. 2018 Aug 10;9(1):3199. doi: 10.1038/s41467-018-05745-w.
[h=1]Nuclear-resident RIG-I senses viral replication inducing antiviral immunity.[/h] Liu G[SUP]1,[/SUP][SUP]2[/SUP], Lu Y[SUP]1,[/SUP][SUP]3[/SUP], Thulasi Raman SN[SUP]1[/SUP], Xu F[SUP]1[/SUP], Wu Q[SUP]1,[/SUP][SUP]3[/SUP], Li Z[SUP]1,[/SUP][SUP]2[/SUP], Brownlie R[SUP]1[/SUP], Liu Q[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Zhou Y[SUP]4,[/SUP][SUP]5,[/SUP][SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
PMID: 30097581 PMCID: PMC6086882 DOI: 10.1038/s41467-018-05745-w
Free PMC Article
[h=1]Nuclear-resident RIG-I senses viral replication inducing antiviral immunity.[/h] Liu G[SUP]1,[/SUP][SUP]2[/SUP], Lu Y[SUP]1,[/SUP][SUP]3[/SUP], Thulasi Raman SN[SUP]1[/SUP], Xu F[SUP]1[/SUP], Wu Q[SUP]1,[/SUP][SUP]3[/SUP], Li Z[SUP]1,[/SUP][SUP]2[/SUP], Brownlie R[SUP]1[/SUP], Liu Q[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Zhou Y[SUP]4,[/SUP][SUP]5,[/SUP][SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
PMID: 30097581 PMCID: PMC6086882 DOI: 10.1038/s41467-018-05745-w
Free PMC Article