Evidence map›Paper›PMID 33540583›Full record

ReviewCells2021

Mechanisms of Coronavirus Nsp1-Mediated Control of Host and Viral Gene Expression.

Keisuke Nakagawa, Shinji Makino

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Structure-function mapping and mechanistic insights on the SARS CoV2 Nsp1.Protein science : a publication of the Protein Society · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. SARS-CoV-2 nsp15 endoribonuclease antagonizes dsRNA-induced antiviral signaling.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
  10. Interaction between coronaviruses and the autophagic response.Frontiers in cellular and infection microbiology · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Keisuke NakagawaLaboratory of Veterinary Microbiology, Joint Department of Veterinary Medicine, Gifu University, Gifu 501-1193, Japan.
Shinji MakinoDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019, USA.
Gifu University · JPThe University of Texas Medical Branch at Galveston · US

Funding

New Paradigm for Host and Viral Gene Regulation by MERS Coronavirus nsp1R01AI114657 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MAKINO, SHINJI · 2015 to 2019
$2.1M
Analysis of SARS Coronavirus-Host Cell InteractionsR01AI072493 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MAKINO, SHINJI · 2007 to 2011
$1.5M
Interplay between coronaviruses and nonsense-mediated mRNA decay pathwayR01AI146081 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MAKINO, SHINJI · 2020 to 2023
$1.2M
National Institute of Allergy and Infectious Diseases AI72493, AI99107, AI114657, AI146081NIAID NIH HHS R01 AI114657NIAID NIH HHS R01 AI146081The University of Texas Medical Branch IHII Pilot grants
6 · The paper itself

Abstract

Many viruses disrupt host gene expression by degrading host mRNAs and/or manipulating translation activities to create a cellular environment favorable for viral replication. Often, virus-induced suppression of host gene expression, including those involved in antiviral responses, contributes to viral pathogenicity. Accordingly, clarifying the mechanisms of virus-induced disruption of host gene expression is important for understanding virus-host cell interactions and virus pathogenesis. Three highly pathogenic human coronaviruses (CoVs), including severe acute respiratory syndrome (SARS)-CoV, Middle East respiratory syndrome (MERS)-CoV, and SARS-CoV-2, have emerged in the past two decades. All of them encode nonstructural protein 1 (nsp1) in their genomes. Nsp1 of SARS-CoV and MERS-CoV exhibit common biological functions for inducing endonucleolytic cleavage of host mRNAs and inhibition of host translation, while viral mRNAs evade the nsp1-induced mRNA cleavage. SARS-CoV nsp1 is a major pathogenic determinant for this virus, supporting the notion that a viral protein that suppresses host gene expression can be a virulence factor, and further suggesting the possibility that SARS-CoV-2 nsp1, which has high amino acid identity with SARS-CoV nsp1, may serve as a major virulence factor. This review summarizes the gene expression suppression functions of nsp1 of CoVs, with a primary focus on SARS-CoV nsp1 and MERS-CoV nsp1.

Indexed as

BetacoronavirusAnimalsCoronavirus InfectionsGene Expression RegulationHost Microbial InteractionsHumansMiceRNA-Dependent RNA PolymeraseRNA, MessengerViral Nonstructural ProteinsVirus ReplicationNsp1 protein, SARS coronavirusRNA-Dependent RNA PolymeraseRNA, MessengerViral Nonstructural Proteinscoronaviruseshost gene expression suppressionmRNA degradationnsp1translational suppressionvirulence factor

Identifiers

PMID33540583
PMCPMC7912902
OpenAlexW3126728910

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.