Splicing suppression alters the STING transcription start site to attenuate antiviral innate immunity.
CrPV virus suppresses STING-mediated antiviral immunity by altering its transcription start site, reducing antiviral isoform production in invertebrates.
- Why it matters: Understanding viral evasion strategies is crucial for comprehending immune defenses across species, especially given the evolutionary conservation of splicing and STING pathways.
- What they did: The study used infection models and gene expression analyses to show that CrPV down-regulates spliceosomal genes, disrupting splicing and shifting STING transcription from antiviral to nonantiviral variants.
- The result: This mechanism weakens the innate immune response, revealing a novel viral immune evasion tactic that may be broadly relevant to immune regulation in diverse organisms.