WP5116 - SARS-CoV-2 B.1.1.7 variant antagonises innate immune activation - Homo sapiens

This pathway describes the antagonistic effects of the SARS-CoV-2 B.1.1.7 (Alpha) variant on innate immune activation. The pathway is based on Figure 5 from [Thorne et al.](https://www.biorxiv.org/content/10.1101/2021.06.06.446826v1.full).

SARS-CoV-2 is known to antagonize innate immune activation, and the highly transmissible B.1.1.7 variant does this more effectively by increased RNA synthesis and increased protein expression of key innate immune antagonists, orf9b, orf6 and N:
N prevents activation of RNA sensor RIG-1 (DDX58), orf6 inhibits IRF3 nuclear translocation and subsequent type 1 interferon production and orf9b inhibits RNA-sensing by binding to TOM70 (TOMM70). The latter interaction is regulated by phosphorylation of orf9b on Ser53; orf9b that is phosphorylated on Ser53 cannot bind to TOM70.