Structural basis for translational shutdown and immune evasion by the Nsp1 protein of SARS-CoV-2

SARS-CoV-2 nonstructural protein 1 (Nsp1) is derived from open reading frame (ORF) 1 that is initially translated after viral entry into host cells. Nsp1 binds to host ribosomal subunit to inhibit mRNA translation. This shutdown event occurs not only in interferon-related genes, but also in several other genes related with multiple cellular event such as autophagy and pro-inflammatory cytokine responses. An interaction between 5'-untranslational region of viral mRNA and Nsp1 prevent shutdown of viral translation, whose mechanism should be further studied.