Evidence map›Paper›PMID 34386498›Full record

ArticleFrontiers in cell and developmental biology2021

ORF3a-Mediated Incomplete Autophagy Facilitates Severe Acute Respiratory Syndrome Coronavirus-2 Replication.

Yafei Qu, Xin Wang, Yunkai Zhu, Weili Wang, Yuyan Wang, Gaowei Hu, Chengrong Liu, Jingjiao Li, Shanhui Ren, Maggie Z X Xiao and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
13.7field-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

71 citing papers in PubMed, 100 citations in OpenAlex.

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  12. Post-Acute Sequelae and Mitochondrial Aberration in SARS-CoV-2 Infection.International journal of molecular sciences · 2024
    Review
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  14. SARS-CoV-2 biology and host interactions.Nature reviews. Microbiology · 2024
    Review
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11 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

17 authors at 6 institutions in 3 countries.

Yafei QuResearch Center of Translational Medicine, Shanghai Institute of Immunology, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xin WangResearch Center of Translational Medicine, Shanghai Institute of Immunology, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yunkai ZhuKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Science, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Weili WangResearch Center of Translational Medicine, Shanghai Institute of Immunology, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuyan WangKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Science, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Gaowei HuKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Science, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Chengrong LiuResearch Center of Translational Medicine, Shanghai Institute of Immunology, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jingjiao LiResearch Center of Translational Medicine, Shanghai Institute of Immunology, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shanhui RenKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Science, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Maggie Z X XiaoFaculty of Medicine, University of Alberta, Edmonton, AB, Canada.
Zhenshan LiuResearch Center of Translational Medicine, Shanghai Institute of Immunology, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chunxia WangDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Joyce FuDepartment of Statistics, University of California, Riverside, Riverside, CA, United States.
Yucai ZhangDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Ping LiKey Laboratory for Food Microbial Technology of Zhejiang Province, Zhejiang Gongshang University, Hangzhou, China.
Rong ZhangKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Science, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Qiming LiangResearch Center of Translational Medicine, Shanghai Institute of Immunology, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shanghai Children's Hospital · CNShanghai Medical College of Fudan University · CNShanghai Jiao Tong University · CNUniversity of Alberta · CAUniversity of California, Riverside · USZhejiang Gongshang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is the causative agent for the coronavirus disease 2019 (COVID-19) pandemic and there is an urgent need to understand the cellular response to SARS-CoV-2 infection. Beclin 1 is an essential scaffold autophagy protein that forms two distinct subcomplexes with modulators Atg14 and UVRAG, responsible for autophagosome formation and maturation, respectively. In the present study, we found that SARS-CoV-2 infection triggers an incomplete autophagy response, elevated autophagosome formation but impaired autophagosome maturation, and declined autophagy by genetic knockout of essential autophagic genes reduces SARS-CoV-2 replication efficiency. By screening 26 viral proteins of SARS-CoV-2, we demonstrated that expression of ORF3a alone is sufficient to induce incomplete autophagy. Mechanistically, SARS-CoV-2 ORF3a interacts with autophagy regulator UVRAG to facilitate PI3KC3-C1 (Beclin-1-Vps34-Atg14) but selectively inhibit PI3KC3-C2 (Beclin-1-Vps34-UVRAG). Interestingly, although SARS-CoV ORF3a shares 72.7% amino acid identity with the SARS-CoV-2 ORF3a, the former had no effect on cellular autophagy response. Thus, our findings provide the mechanistic evidence of possible takeover of host autophagy machinery by ORF3a to facilitate SARS-CoV-2 replication and raise the possibility of targeting the autophagic pathway for the treatment of COVID-19.

Indexed as

autophagyCOVID-19ORF3aSARS-CoV-2UVRAG

Identifiers

PMID34386498
PMCPMC8353283
OpenAlexW3186709926

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.