When RNA viruses attack the cells, the RIG-I-like receptors or Toll-like receptors sense pathogen-associated molecular patterns, and signal downstream through interferon regulatory factors (IRFs), transcription factors induce synthesis of type I and type III interferons. RNA viruses have evolved sophisticated strategies to disrupt these signalling pathways and evade elimination by cells. So it is important to know how IRFs maintain basal levels of protection against viruses.
The researchers from University of North Carolina at Chapel Hill and Tokyo Metropolitan Institute of Medicine depleted antiviral factors linked to RIG-I-like receptor and Toll-like receptor signalling to map critical host pathways restricting positive-strand RNA virus replication in immortalized hepatocytes and identified an unexpected role for IRF1. The results showed that constitutively expressed IRF1 acts independently of mitochondrial antiviral signalling (MAVS) protein, IRF3 and signal transducer and activator of transcription 1 (STAT1)-dependent signalling to provide intrinsic antiviral protection in actinomycin D-treated cells.
IRF1 localizes to the nucleus, where it maintains the basal transcription of a suite of antiviral genes that protect against multiple pathogenic RNA viruses, including hepatitis A and C viruses, Zika virus and dengue virus. The IRF1 protein in hepatocytes regulates RARRES3, an enzyme that attacks the virus when it is attempted to express in cells.
“Our findings reveal an unappreciated layer of hepatocyte-intrinsic immunity to these positive-strand RNA viruses and identify previously unrecognized antiviral effector genes.” the researcher said.
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