Evidence map›Paper›PMID 35005526›Full record

ArticleiScience2022

ACE2 can act as the secondary receptor in the FcγR-dependent ADE of SARS-CoV-2 infection.

Zai Wang, Tingting Deng, Yulian Zhang, Wenquan Niu, Qiangqiang Nie, Shengnan Yang, Peipei Liu, Pengfei Pei, Long Chen, Haibo Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 36 citations in OpenAlex.

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  17. Spike mutation resilient scFv76 antibody counteracts SARS-CoV-2 lung damage upon aerosol delivery.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  18. Multifaceted roles of Fcγ receptors in COVID-19 and vaccine responses.American journal of translational research · 2023
    Review
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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

11 authors at 6 institutions in 1 country.

Zai WangInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China.
Tingting DengInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China.
Yulian ZhangDepartment of Neurosurgery, Peking University China-Japan Friendship School of Clinical Medicine, Beijing, China.
Wenquan NiuInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China.
Qiangqiang NieDepartment of Cardiovascular Surgery, China-Japan Friendship Hospital, Beijing, China.
Shengnan YangDepartment of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, China-Japan Friendship Hospital, Beijing, China.
Peipei LiuDepartment of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, China-Japan Friendship Hospital, Beijing, China.
Pengfei PeiBeijing Key Laboratory of Bioprocess, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, China.
Long ChenBeijing Key Laboratory of Bioprocess, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, China.
Haibo LiDepartment of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, China-Japan Friendship Hospital, Beijing, China.
Bin CaoDepartment of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, China-Japan Friendship Hospital, Beijing, China.
China-Japan Friendship Hospital · CNBeijing University of Chemical Technology · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNCapital Medical University · CNHarbin Medical University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is unknown whether antibody-mediated enhancement (ADE) contributes to the pathogenesis of COVID-19, and the conditions for ADE needs to be elucidated. We demonstrated that without inducing an ACE2-independent ADE on Raji cells, the neutralizing antibody CB6, a mouse anti-S1 serum and convalescent plasma, induced ADE on cells expressing FcγRIIA/CD32A and low levels of endogenous ACE2. ADE occurred at sub-neutralizing antibody concentrations, indicating that unneutralized S protein was required for ADE. The enhanced infectivity of 614G variant was higher than that of 614D wildtype in the presence of antibodies, further suggesting that ADE may be influenced by virus strains with different ACE2-binding affinity. Finally, knockdown of ACE2 or treatment with a fusion-inhibition peptide EK1C4 significantly reduced ADE. In conclusion, we identified an ADE mechanism mediated by neutralizing antibodies against SARS-CoV-2. ACE2 may act as a secondary receptor required for the antibody- and FcγR-mediated enhanced entry of SARS-CoV-2.

Indexed as

ImmunologyVirology

Identifiers

PMID35005526
PMCPMC8719361
OpenAlexW4206411709

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.