Evidence map›Paper›PMID 32038520›Full record

ArticleFrontiers in microbiology2019

Regulation of the ER Stress Response by the Ion Channel Activity of the Infectious Bronchitis Coronavirus Envelope Protein Modulates Virion Release, Apoptosis, Viral Fitness, and Pathogenesis.

Shumin Li, Lixia Yuan, Guo Dai, Rui Ai Chen, Ding Xiang Liu, To Sing Fung

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
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  7. Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025
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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

6 authors at 2 institutions in 1 country.

Shumin LiGuangdong Province Key Laboratory of Microbial Signals & Disease Control, and Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou, China.
Lixia YuanGuangdong Province Key Laboratory of Microbial Signals & Disease Control, and Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou, China.
Guo DaiGuangdong Province Key Laboratory of Microbial Signals & Disease Control, and Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou, China.
Rui Ai ChenCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, China.
Ding Xiang LiuGuangdong Province Key Laboratory of Microbial Signals & Disease Control, and Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou, China.
To Sing FungGuangdong Province Key Laboratory of Microbial Signals & Disease Control, and Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou, China.
South China Agricultural University · CNZhaoqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus (CoV) envelope (E) protein is a small structural protein critical for virion morphogenesis and release. The recently characterized E protein ion channel activity (EIC) has also been implicated in modulating viral pathogenesis. In this study, we used infectious bronchitis coronavirus (IBV) as a model to study EIC. Two recombinant IBVs (rIBVs) harboring EIC-inactivating mutations - rT16A and rA26F - were serially passaged, and several compensatory mutations were identified in the transmembrane domain (TMD). Two rIBVs harboring these putative EIC-reverting mutations - rT16A/A26V and rA26F/F14N - were recovered. Compared with the parental rIBV-p65 control, all four EIC mutants exhibited comparable levels of intracellular RNA synthesis, structural protein production, and virion assembly. Our results showed that the IBV EIC contributed to the induction of ER stress response, as up-regulation of ER stress-related genes was markedly reduced in cells infected with the EIC-defective mutants. EIC-defective mutants also formed smaller plaques, released significantly less infectious virions into the culture supernatant, and had lower levels of viral fitness in cell culture. Significantly, all these defective phenotypes were restored in cells infected with the putative EIC revertants. EIC mutations were also implicated in regulating IBV-induced apoptosis, induction of pro-inflammatory cytokines, and viral pathogenicity

Indexed as

coronavirusER stress responseion channel activitypathogenesispro-inflammatory cytokineviroporin

Identifiers

PMID32038520
PMCPMC6992538
OpenAlexW3002589413

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.