ArticleInfection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases2010
Nsp1 proteins of group I and SARS coronaviruses share structural and functional similarities.
Article in Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Strategic variations in sarbecovirus and merbecovirus Nsp1 linker regions for translation inhibition.Nucleic acids research · 2026Article
- Human Coronavirus-229E Hijacks Key Host-Cell RNA-Processing Complexes for Replication.Journal of proteome research · 2025Article
- Characterization of Gene Expression Suppression by Bovine Coronavirus Non-Structural Protein 1.Viruses · 2025Article
- SARS-CoV-2 nsp1 mediates broad inhibition of translation in mammals.Cell reports · 2025Article
- Anti-interferon armamentarium of human coronaviruses.Cellular and molecular life sciences : CMLS · 2025Review
- HCoV-229E Mpro Suppresses RLR-Mediated Innate Immune Signalling Through Cleavage of NEMO and Through Other Mechanisms.International journal of molecular sciences · 2025Article
- PEDV evades MHC-I-related immunity through nsp1-mediated NLRC5 translation inhibition.Journal of virology · 2024Article
- SARS-CoV2 Nsp1 is a metal-dependent DNA and RNA endonuclease.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Article
- The art of hijacking: how Nsp1 impacts host gene expression during coronaviral infections.Biochemical Society transactions · 2024Review
- Coronavirus takeover of host cell translation and intracellular antiviral response: a molecular perspective.The EMBO journal · 2024Review
- An Evolutionarily Conserved Strategy for Ribosome Binding and Host Translation Inhibition by β-coronavirus Non-structural Protein 1.Journal of molecular biology · 2023Article
- An evolutionarily conserved strategy for ribosome binding and inhibition by β-coronavirus non-structural protein 1.bioRxiv : the preprint server for biology · 2023Article
- Molecular mechanisms of human coronavirus NL63 infection and replication.Virus research · 2023Review
- Article
- The Role of Viral RNA Degrading Factors in Shutoff of Host Gene Expression.Annual review of virology · 2022Review
- Viral and cellular translation during SARS-CoV-2 infection.FEBS open bio · 2022Review
- Control of Innate Immune Activation by Severe Acute Respiratory Syndrome Coronavirus 2 and Other Coronaviruses.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2021Review
- Review
- Coronavirus Nsp1: Immune Response Suppression and Protein Expression Inhibition.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nsp1 protein of the highly pathogenic SARS coronavirus suppresses host protein synthesis, including genes involved in the innate immune system. A bioinformatic analysis revealed that the nsp1 proteins of group I and SARS coronaviruses have similar structures. Nsp1 proteins of group I coronaviruses interacted with host ribosomal 40S subunit and did not inhibit IRF-3 activation. However, synthesis of host immune and non-immune proteins was inhibited by nsp1 proteins at both transcriptional and translational levels, similar to SARS coronavirus nsp1. These results indicate that different coronaviruses might employ the same nsp1 mechanism to antagonize host innate immunity and cell proliferation. However, nsp1 may not be the key determinant of viral pathogenicity, or the factor used by the SARS coronavirus to evade host innate immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.