Evidence map›Paper›PMID 33372174›Full record

ArticleSignal transduction and targeted therapy2020

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) membrane (M) protein inhibits type I and III interferon production by targeting RIG-I/MDA-5 signaling.

Yi Zheng, Meng-Wei Zhuang, Lulu Han, Jing Zhang, Mei-Ling Nan, Peng Zhan, Dongwei Kang, Xinyong Liu, Chengjiang Gao, Pei-Hui Wang

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 2 pooled it
19.3field-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

224 citing papers in PubMed, 2 syntheses or guidelines pooled it, 299 citations in OpenAlex.

  1. COVID-19 pandemic: the delta variant, T-cell responses, and the efficacy of developing vaccines.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
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164 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

10 authors at 1 institution in 1 country.

Yi ZhengKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, 250012, Jinan, China.
Meng-Wei ZhuangKey Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, 250012, Jinan, China.
Lulu HanKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, 250012, Jinan, China.
Jing ZhangKey Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, 250012, Jinan, China.
Mei-Ling NanKey Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, 250012, Jinan, China.
Peng ZhanDepartment of Medicinal Chemistry, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 West Culture Road, 250012, Jinan, Shandong, PR China.
Dongwei KangDepartment of Medicinal Chemistry, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 West Culture Road, 250012, Jinan, Shandong, PR China.ORCID 0000-0001-9232-953X
Xinyong LiuDepartment of Medicinal Chemistry, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 West Culture Road, 250012, Jinan, Shandong, PR China.
Chengjiang GaoKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, 250012, Jinan, China. cgao@sdu.edu.cn.
Pei-Hui WangKey Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, 250012, Jinan, China. pei-hui.wang@connect.hku.hk.ORCID 0000-0001-6853-2423
Shandong University · CN

Funding

China Postdoctoral Science Foundation 2018M642662National Natural Science Foundation of China (National Science Foundation of China) 31730026National Natural Science Foundation of China (National Science Foundation of China) 81525012National Natural Science Foundation of China (National Science Foundation of China) 81901604National Natural Science Foundation of China (National Science Foundation of China) 81930039Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation) SBK2020042706
6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has quickly spread worldwide and has affected more than 10 million individuals. A typical feature of COVID-19 is the suppression of type I and III interferon (IFN)-mediated antiviral immunity. However, the molecular mechanism by which SARS-CoV-2 evades antiviral immunity remains elusive. Here, we reported that the SARS-CoV-2 membrane (M) protein inhibits the production of type I and III IFNs induced by the cytosolic dsRNA-sensing pathway mediated by RIG-I/MDA-5-MAVS signaling. In addition, the SARS-CoV-2 M protein suppresses type I and III IFN induction stimulated by SeV infection or poly (I:C) transfection. Mechanistically, the SARS-CoV-2 M protein interacts with RIG-I, MAVS, and TBK1, thus preventing the formation of the multiprotein complex containing RIG-I, MAVS, TRAF3, and TBK1 and subsequently impeding the phosphorylation, nuclear translocation, and activation of IRF3. Consequently, ectopic expression of the SARS-CoV-2 M protein facilitates the replication of vesicular stomatitis virus. Taken together, these results indicate that the SARS-CoV-2 M protein antagonizes type I and III IFN production by targeting RIG-I/MDA-5 signaling, which subsequently attenuates antiviral immunity and enhances viral replication. This study provides insight into the interpretation of SARS-CoV-2-induced antiviral immune suppression and illuminates the pathogenic mechanism of COVID-19.

Indexed as

Signal TransductionAnimalsChlorocebus aethiopsCoronavirus M ProteinsCOVID-19DEAD Box Protein 58HEK293 CellsHeLa CellsHumansInterferon-Induced Helicase, IFIH1Interferon LambdaInterferonsInterferon Type IReceptors, ImmunologicSARS-CoV-2Vero CellsCoronavirus M ProteinsDEAD Box Protein 58IFIH1 protein, humanInterferon-Induced Helicase, IFIH1Interferon LambdaInterferonsInterferon Type Imembrane protein, SARS-CoV-2Receptors, ImmunologicRIGI protein, humanViral Matrix Proteins

Identifiers

PMID33372174
PMCPMC7768267
OpenAlexW3115832826

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.