RIG-I-like receptors articles from across Nature Portfolio

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.

The RIG-I like receptors sense RNA viruses and initiate antiviral immunity. Here the authors screen 375 definite ubiquitin ligases and propose UBR5 promotes RLR transcription by disengaging the TRIM28-imposed brake on the RLR promoters.

Riplet conjugates K63-Ub chain to RIG-I in order to induce a robust antiviral response, but the mechanism of action remains unclear. Here, the authors show that Riplet recognizes RIG-I regardless of its RNA-bound status and promotes RIG-I signaling independent of RIG-I oligomerization.

Variation in infection dynamics and host cell sensing kinetics shape human antiviral response.

Disturbance of the cell cytoskeleton is a necessary priming step for activation of the RIG-I-like receptors.

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.