Evidence map›Paper›PMID 30297408›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Interplay between coronavirus, a cytoplasmic RNA virus, and nonsense-mediated mRNA decay pathway.

Masami Wada, Kumari G Lokugamage, Keisuke Nakagawa, Krishna Narayanan, Shinji Makino

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 109 citations in OpenAlex.

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  19. Gene Expression Risk Scores for COVID-19 Illness Severity.The Journal of infectious diseases · 2023
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3 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Masami WadaDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019.
Kumari G LokugamageDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019.
Keisuke NakagawaDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019.
Krishna NarayananDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019.
Shinji MakinoDepartment of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1019; shmakino@utmb.edu.
The 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 Coronavirus-Host Cell InteractionsR01AI099107 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MAKINO, SHINJI · 2012 to 2016
$2.0M
NIAID NIH HHS R01 AI099107NIAID NIH HHS R01 AI114657
6 · The paper itself

Abstract

Coronaviruses (CoVs), including severe acute respiratory syndrome CoV and Middle East respiratory syndrome CoV, are enveloped RNA viruses that carry a large positive-sense single-stranded RNA genome and cause a variety of diseases in humans and domestic animals. Very little is known about the host pathways that regulate the stability of CoV mRNAs, which carry some unusual features. Nonsense-mediated decay (NMD) is a eukaryotic RNA surveillance pathway that detects mRNAs harboring aberrant features and targets them for degradation. Although CoV mRNAs are of cytoplasmic origin, the presence of several NMD-inducing features (including multiple ORFs with internal termination codons that create a long 3' untranslated region) in CoV mRNAs led us to explore the interplay between the NMD pathway and CoVs. Our study using murine hepatitis virus as a model CoV showed that CoV mRNAs are recognized by the NMD pathway as a substrate, resulting in their degradation. Furthermore, CoV replication induced the inhibition of the NMD pathway, and N protein (a viral structural protein) had an NMD inhibitory function that protected viral mRNAs from rapid decay. Our data further suggest that the NMD pathway interferes with optimal viral replication by degrading viral mRNAs early in infection, before sufficient accumulation of N protein. Our study presents clear evidence for the biological importance of the NMD pathway in controlling the stability of mRNAs and the efficiency of replication of a cytoplasmic RNA virus.

Indexed as

3' Untranslated RegionsAnimalsCoronavirusCytoplasmMiceNonsense Mediated mRNA DecayOpen Reading FramesRNA, MessengerRNA StabilityRNA VirusesVirus Replication3' Untranslated RegionsRNA, Messengercoronaviruscytoplasmic RNA virusinhibition of NMDlong 3′ UTRnonsense-mediated mRNA decay

Identifiers

PMID30297408
PMCPMC6205489
OpenAlexW2895829670

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.