Evidence map›Paper›PMID 35313595›Full record

ArticlebioRxiv : the preprint server for biology2022

Parsing the role of NSP1 in SARS-CoV-2 infection.

Tal Fisher, Avi Gluck, Krishna Narayanan, Makoto Kuroda, Aharon Nachshon, Jason C Hsu, Peter J Halfmann, Yfat Yahalom-Ronen, Yaara Finkel, Michal Schwartz and 7 more

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed, 4 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 5 institutions in 3 countries.

Tal FisherDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Avi GluckDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Krishna NarayananDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019, USA.
Makoto KurodaDepartment of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53711, USA.
Aharon NachshonDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Jason C HsuDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019, USA.
Peter J HalfmannDepartment of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53711, USA.
Yfat Yahalom-RonenDepartment of Infectious Diseases, Israel Institute for Biological Research, Ness Ziona 74100, Israel.
Yaara FinkelDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Michal SchwartzDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Shay WeissDepartment of Infectious Diseases, Israel Institute for Biological Research, Ness Ziona 74100, Israel.
Chien-Te K TsengDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019, USA.
Tomer IsraelyDepartment of Infectious Diseases, Israel Institute for Biological Research, Ness Ziona 74100, Israel.
Nir ParanDepartment of Infectious Diseases, Israel Institute for Biological Research, Ness Ziona 74100, Israel.
Yoshihiro KawaokaDepartment of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53711, USA.
Shinji MakinoDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019, USA.
Noam Stern-GinossarDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Weizmann Institute of Science · ILIsrael Institute for Biological Research · ILThe University of Texas Medical Branch at Galveston · USUniversity of Wisconsin–Madison · USTokyo Medical University · JP

Funding

Interplay between coronaviruses and nonsense-mediated mRNA decay pathwayR01AI146081 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MAKINO, SHINJI · 2020 to 2023
$1.2M
NIAID NIH HHS HHSN272201400008CNIAID NIH HHS R01 AI146081
6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the ongoing coronavirus disease 19 (COVID-19) pandemic. Despite its urgency, we still do not fully understand the molecular basis of SARS-CoV-2 pathogenesis and its ability to antagonize innate immune responses. SARS-CoV-2 leads to shutoff of cellular protein synthesis and over-expression of nsp1, a central shutoff factor in coronaviruses, inhibits cellular gene translation. However, the diverse molecular mechanisms nsp1 employs as well as its functional importance in infection are still unresolved. By overexpressing various nsp1 mutants and generating a SARS-CoV-2 mutant in which nsp1 does not bind ribosomes, we untangle the effects of nsp1. We uncover that nsp1, through inhibition of translation and induction of mRNA degradation, is the main driver of host shutoff during SARS-CoV-2 infection. Furthermore, we find the propagation of nsp1 mutant virus is inhibited specifically in cells with intact interferon (IFN) response as well as

Identifiers

PMID35313595
PMCPMC8936099
OpenAlexW4220906160

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.