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© Thomas Wollert
Publication : PLoS pathogens

Virus subtype-specific suppression of MAVS aggregation and activation by PB1-F2 protein of influenza A (H7N9) virus.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in PLoS pathogens - 01 Jun 2020

Cheung PH, Lee TT, Kew C, Chen H, Yuen KY, Chan CP, Jin DY,

Link to Pubmed [PMID] – 32511263

Link to DOI – 10.1371/journal.ppat.1008611

PLoS Pathog 2020 06; 16(6): e1008611

Human infection with avian influenza A (H5N1) and (H7N9) viruses causes severe respiratory diseases. PB1-F2 protein is a critical virulence factor that suppresses early type I interferon response, but the mechanism of its action in relation to high pathogenicity is not well understood. Here we show that PB1-F2 protein of H7N9 virus is a particularly potent suppressor of antiviral signaling through formation of protein aggregates on mitochondria and inhibition of TRIM31-MAVS interaction, leading to prevention of K63-polyubiquitination and aggregation of MAVS. Unaggregated MAVS accumulated on fragmented mitochondria is prone to degradation by both proteasomal and lysosomal pathways. These properties are proprietary to PB1-F2 of H7N9 virus but not shared by its counterpart in WSN virus. A recombinant virus deficient of PB1-F2 of H7N9 induces more interferon β in infected cells. Our findings reveal a subtype-specific mechanism for destabilization of MAVS and suppression of interferon response by PB1-F2 of H7N9 virus.

https://pubmed.ncbi.nlm.nih.gov/32511263