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RIG-I-like receptors (retinoic acid-inducible gene I-like receptors, RLRs) are a family of molecules that are expressed inside cells in order to sense viruses. They recognise double-stranded RNA molecules that are produced by certain viruses and can induce antiviral immune responses.
Wang and colleagues show that in skeletal muscle cells and cardiomyocytes, the glucose transporter GLUT4 is a negative regulator of RIG-I-like receptor signaling during viral infection by redistributing RIG-I and MDA5 to the plasma membrane and attenuating interferon responses.
O’Carroll and Peace et al. provide a mechanism for the induction of type I interferons by the immunomodulatory compound itaconate, which involves inhibition of succinate dehydrogenase and release of mitochondrial double-stranded RNA.
The RNA exonuclease REXO2 plays an important role in the degradation of mitochondrial RNA. Authors here describe a dominant negative REXO2 mutation that causes autoinflammatory disease via Type I IFN activation.
The use of oncolytic viruses as a therapy for cancer is limited by mechanisms inhibiting viral replication in the tumor. Here, the authors show that a chemical derivative of itaconate, 4-octyl itaconate, increases oncolytic virus VSVΔ51 efficacy in various cancer models, through decreasing antiviral immunity.
The POLG1 mutation p.W748S, which is associated with mitochondrial recessive ataxia syndrome, dampens innate immune responses by compromising mtDNA replisome stability, and this explains why a viral infection can trigger the development of the disease and contribute to its variable clinical manifestation.
Itaconate is an immunomodulatory metabolite that influences the outcome of infections and inflammatory diseases. New evidence indicates that itaconate-induced inhibition of succinate dehydrogenase regulates type 1 interferon production via the release of mitochondrial RNA, linking TCA cycle modulation to antiviral interferon responses.
Takashi Fujita’s discovery of RNA helicases as intracellular viral replication sensors illustrates how scientific knowledge develops in logical — and sometimes illogical — ways.
The virome, increasingly recognized as a critical component of the mammalian microbiota, modulates host physiology. An antiviral treatment approach reveals that, via RIG-I signaling, the commensal virome is essential for the homeostasis of intestinal intraepithelial lymphocytes.
