Cheng Huang

TL;DR: expression of nsp1, the most N-terminal gene 1 protein, prevented Sendai virus-induced endogenous IFN-β mRNA accumulation without inhibiting dimerization of IFN regulatory factor 3, a protein that is essential for activation of theIFN- β promoter.

TL;DR: It is demonstrated that SARS-CoV nsp1 suppressed host innate immune functions, including type I IFN expression, in infected cells and suggested that Sars- CoV nSp1 most probably plays a critical role in SARS -CoV virulence.

TL;DR: The sensitivity of SARS-CoV-2 to recombinant human interferons α and β (IFNα/β) is reported and the potential efficacy of human Type I IFN in suppressing Sars- CoV- 2 infection is demonstrated, which could inform future treatment options for COVID-19.

TL;DR: Nsp1 induced RNA cleavage in templates carrying the internal ribosome entry site (IRES) from encephalomyocarditis virus, but not in those carrying IRES elements from hepatitis C or cricket paralysis viruses, demonstrating that the nsp1-induced RNA modification was template-dependent.

TL;DR: It is revealed that the nsp1 induced endonucleolytic RNA cleavage mainly near the 5′ untranslated region of capped mRNA templates, which may be an important strategy by which the virus circumvents the action of nsp 1 leading to the efficient accumulation of viral mRNAs and viral proteins during infection.