Back

SARS-CoV-2 impairs interferon production via NSP2-induced repression of mRNA translation

Choi, J.-H.; Zhang, X.; Zhang, C.; Dai, D. L.; Luo, J.; Ladak, R.; Li, Q.; Wiebe, S.; Liu, A. C. H.; Ran, X.; Yang, J.; Naeli, P.; Garzia, A.; Zhou, L.; Mahmood, N.; Deng, Q.; Elaish, M.; Lin, R.; Hobman, T.; Pelletier, J.; Alain, T.; Vidal, S.; Duchaine, T.; Mazhab-Jafari, M.; Mao, X.; Jafarnejad, S. M.; Sonenberg, N.

2022-01-20 microbiology
10.1101/2022.01.19.476693 bioRxiv
Show abstract

Viruses evade the innate immune response by suppressing the production or activity of cytokines such as type I interferons (IFNs). Here we report the discovery of a novel mechanism by which the SARS-CoV-2 virus co-opts an intrinsic cellular machinery to suppress the production of the key immunostimulatory cytokine IFN-{beta}. We reveal that the SARS-CoV-2 encoded Non-Structural Protein 2 (NSP2) directly interacts with the cellular GIGYF2 protein. This interaction enhances the binding of GIGYF2 to the mRNA cap-binding protein 4EHP, thereby repressing the translation of the Ifnb1 mRNA. Depletion of GIGYF2 or 4EHP significantly enhances IFN-{beta} production, leading to reduced viral infection. Our findings reveal a new target for rescuing the antiviral innate immune response to SARS-CoV-2 and other RNA viruses.

Matching journals

The top 2 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.