Evidence map›Paper›PMID 33760889›Full record

ArticlePLoS pathogens2021

Comparative analysis reveals the species-specific genetic determinants of ACE2 required for SARS-CoV-2 entry.

Wenlin Ren, Yunkai Zhu, Yuyan Wang, Hongyang Shi, Yin Yu, Gaowei Hu, Fei Feng, Xiaomin Zhao, Jun Lan, Jianping Wu and 10 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.9field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

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  8. Adaptation of SARS-CoV-2 to ACE2Journal of virology · 2024
    Article
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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

20 authors at 7 institutions in 2 countries.

Wenlin RenCenter for Infectious Disease Research, School of Medicine, Tsinghua University, Beijing, China.ORCID 0000-0002-7290-0935
Yunkai ZhuKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Yuyan WangKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Hongyang ShiCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Yin YuKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, 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 Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Fei FengKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Xiaomin ZhaoCenter for Infectious Disease Research, School of Medicine, Tsinghua University, Beijing, China.
Jun LanSchool of Life Sciences, Tsinghua University, Beijing, China.ORCID 0000-0001-5550-2946
Jianping WuZhejiang Provincial Laboratory of Life Sciences and Biomedicine, Key Laboratory of Structural Biology of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.ORCID 0000-0001-9869-7691
Devin J KenneyDepartment of Microbiology, National Emerging Infectious Diseases Laboratories, Boston University School of Medicine, Boston, Massachusetts, United States of America.ORCID 0000-0002-8758-1930
Florian DouamDepartment of Microbiology, National Emerging Infectious Diseases Laboratories, Boston University School of Medicine, Boston, Massachusetts, United States of America.ORCID 0000-0002-4791-6767
Yimin TongCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Jin ZhongCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-3554-1275
Youhua XieKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Xinquan WangSchool of Life Sciences, Tsinghua University, Beijing, China.ORCID 0000-0003-3136-8070
Zhenghong YuanKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Dongming ZhouDepartment of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.ORCID 0000-0002-5989-7591
Rong ZhangKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China.ORCID 0000-0003-2941-4808
Qiang DingCenter for Infectious Disease Research, School of Medicine, Tsinghua University, Beijing, China.ORCID 0000-0002-6226-869X
Shanghai Medical College of Fudan University · CNChinese Academy of Sciences · CNTsinghua University · CNBeijing Advanced Sciences and Innovation Center · CNBoston University · USTianjin Medical University · CNWestlake University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus interaction with its viral receptor is a primary genetic determinant of host range and tissue tropism. SARS-CoV-2 utilizes ACE2 as the receptor to enter host cell in a species-specific manner. We and others have previously shown that ACE2 orthologs from New World monkey, koala and mouse cannot interact with SARS-CoV-2 to mediate viral entry, and this defect can be restored by humanization of the restrictive residues in New World monkey ACE2. To better understand the genetic determinants behind the ability of ACE2 orthologs to support viral entry, we compared koala and mouse ACE2 sequences with that of human and identified the key residues in koala and mouse ACE2 that restrict viral receptor activity. Humanization of these critical residues rendered both koala and mouse ACE2 capable of binding the spike protein and facilitating viral entry. Our study shed more lights into the genetic determinants of ACE2 as the functional receptor of SARS-CoV-2, which facilitates our understanding of viral entry.

Indexed as

AnimalsBase SequenceCOVID-19Host SpecificityHumansMicePeptidyl-Dipeptidase APhascolarctidaeReceptors, VirusSARS-CoV-2Sequence AlignmentSpike Glycoprotein, CoronavirusVirus InternalizationPeptidyl-Dipeptidase AReceptors, VirusSpike Glycoprotein, Coronavirus

Identifiers

PMID33760889
PMCPMC7990223
OpenAlexW3138856383

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.