Evidence map›Paper›PMID 34845370›Full record

ArticleCellular & molecular immunology2022

SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy.

Xingyu Li, Peili Hou, Wenqing Ma, Xuefeng Wang, Hongmei Wang, Zhangping Yu, Huasong Chang, Tiecheng Wang, Song Jin, Xue Wang and 7 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
12.8field-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

148 citing papers in PubMed, 211 citations in OpenAlex.

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  15. Role of autophagy in antiviral innate immunity.Cellular & molecular biology letters · 2026
    Review
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88 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 2 institutions in 1 country.

Xingyu Li *Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Peili Hou *Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Wenqing Ma *Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Xuefeng Wang *Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, People's Republic of China.
Hongmei WangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China. hongmeiwang@sdnu.edu.cn.
Zhangping YuRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Huasong ChangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Tiecheng WangChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, People's Republic of China.
Song JinRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Xue WangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Wenqi WangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Yudong ZhaoChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, People's Republic of China.
Yong ZhaoChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, People's Republic of China.
Chunqing XuRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Xiaomei MaRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China.
Yuwei GaoChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, People's Republic of China. yuwei0901@outlook.com.
Hongbin HeRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, People's Republic of China. hongbinhe@sdnu.edu.cn.
Shandong Normal University · CNChinese Academy of Agricultural Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The global coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused severe morbidity and mortality in humans. It is urgent to understand the function of viral genes. However, the function of open reading frame 10 (ORF10), which is uniquely expressed by SARS-CoV-2, remains unclear. In this study, we showed that overexpression of ORF10 markedly suppressed the expression of type I interferon (IFN-I) genes and IFN-stimulated genes. Then, mitochondrial antiviral signaling protein (MAVS) was identified as the target via which ORF10 suppresses the IFN-I signaling pathway, and MAVS was found to be degraded through the ORF10-induced autophagy pathway. Furthermore, overexpression of ORF10 promoted the accumulation of LC3 in mitochondria and induced mitophagy. Mechanistically, ORF10 was translocated to mitochondria by interacting with the mitophagy receptor Nip3-like protein X (NIX) and induced mitophagy through its interaction with both NIX and LC3B. Moreover, knockdown of NIX expression blocked mitophagy activation, MAVS degradation, and IFN-I signaling pathway inhibition by ORF10. Consistent with our observations, in the context of SARS-CoV-2 infection, ORF10 inhibited MAVS expression and facilitated viral replication. In brief, our results reveal a novel mechanism by which SARS-CoV-2 inhibits the innate immune response; that is, ORF10 induces mitophagy-mediated MAVS degradation by binding to NIX.

Indexed as

Open Reading FramesSignal TransductionAdaptor Proteins, Signal TransducingAntiviral AgentsAutophagyCOVID-19Gene SilencingHEK293 CellsHeLa CellsHumansImmunity, InnateInterferon Type IMitochondriaMitophagyProteasome Endopeptidase ComplexSARS-CoV-2Adaptor Proteins, Signal TransducingAntiviral AgentsInterferon Type IProteasome Endopeptidase ComplexViral ProteinsMAVSmitophagyNIXORF10SARS-CoV-2

Identifiers

PMID34845370
PMCPMC8628139
OpenAlexW3217099294

What OpenQuestion holds

Textmetadata
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.