TRIM21 mediates rapid uncoating of antibody-opsonized viruses, exposing viral genomes to cytosolic sensors cGAS and RIG-I to trigger early innate immune responses.
Answers are grounded in this paper and cite their sources.
May inform antibody-enhanced antiviral strategies; leaves open clinical translation in human infections.
Encapsidation is a strategy almost universally employed by viruses to protect their genomes from degradation and from innate immune sensors. We show that TRIM21, which targets antibody-opsonized virions for proteasomal destruction, circumvents this protection, enabling the rapid detection and degradation of viral genomes before their replication. TRIM21 triggers an initial wave of cytokine transcription that is antibody, rather than pathogen, driven. This early response is augmented by a second transcriptional program, determined by the nature of the infecting virus. In this second response, TRIM21-induced exposure of the viral genome promotes sensing of DNA and RNA viruses by cGAS and RIG-I. This mechanism allows early detection of an infection event and drives an inflammatory response in mice within hours of viral challenge.
No takes yet. Share an insight, caveat, or question.
Watkinson et al. (2015) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: