SARS-CoV-2 targets ribosomal RNA biogenesis.

Publication date: Feb 29, 2024

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hinders host gene expression, curbing defenses and licensing viral protein synthesis and virulence. During SARS-CoV-2 infection, the virulence factor non-structural protein 1 (Nsp1) targets the mRNA entry channel of mature cytoplasmic ribosomes, limiting translation. We show that Nsp1 also restrains translation by targeting nucleolar ribosome biogenesis. SARS-CoV-2 infection disrupts 18S and 28S ribosomal RNA (rRNA) processing. Expression of Nsp1 recapitulates the processing defects. Nsp1 abrogates rRNA production without altering the expression of critical processing factors or nucleolar organization. Instead, Nsp1 localizes to the nucleolus, interacting with precursor-rRNA and hindering its maturation separately from the viral protein’s role in restricting mature ribosomes. Thus, SARS-CoV-2 Nsp1 limits translation by targeting ribosome biogenesis and mature ribosomes. These findings revise our understanding of how SARS-CoV-2 Nsp1 controls human protein synthesis, suggesting that efforts to counter Nsp1’s effect on translation should consider the protein’s impact from ribosome manufacturing to mature ribosomes.

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Concepts Keywords
Coronavirus CP: Microbiology
Hindering Molecular biology
Host non-structural protein 1 (Nsp1)
Proteins nucleolus
Virulence ribosomal RNA (rRNA)
ribosome biogenesis
RNA processing


Type Source Name
disease VO Severe acute respiratory syndrome coronavirus 2
disease IDO host
disease IDO virulence
disease MESH SARS-CoV-2 infection
pathway REACTOME SARS-CoV-2 Infection
disease MESH defects
disease IDO production
disease VO organization
pathway KEGG Ribosome

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