The lab is happy to have contributed to a new preprint – The SARS-CoV-2 protein ORF3C is a mitochondrial modulator of innate immunity, led by Dr Hazel Stewart from the Firth lab. In this work, the localisation and role of the ORF3C accessory protein encoded by SARS-CoV-2 is explored. Here we show that ORF3c localises to mitochondria during infection, where it inhibits innate immunity by restricting IFN-β production, but not NF-κB activation or JAK-STAT signalling downstream of type I IFN stimulation. We find that ORF3c acts after stimulation with cytoplasmic RNA helicases RIG-I or MDA5 or adaptor protein MAVS, but not after TRIF, TBK1 or phospho-IRF3 stimulation. ORF3c co-immunoprecipitates with the antiviral proteins MAVS and PGAM5 and induces MAVS cleavage by caspase-3. Together, these data provide insight into an uncharacterised mechanism of innate immune evasion by this important human pathogen.
You can read the article on bioRxiv by clicking: here
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