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

被引：27

作者：

Wang, Zai ^{[3
]}

Deng, Tingting ^{[3
]}

Zhang, Yulian ^{[4
,5
]}

Niu, Wenquan ^{[3
]}

Nie, Qiangqiang ^{[6
]}

Yang, Shengnan ^{[1
,2
,7
,8
]}

Liu, Peipei ^{[1
,2
,9
]}

Pei, Pengfei ^{[10
]}

Chen, Long ^{[10
]}

Li, Haibo ^{[1
,2
]}

Cao, Bin ^{[1
,2
,11
,12
]}

机构：

[1] China Japan Friendship Hosp, Natl Clin Res Ctr Resp Dis, Ctr Resp Med, Dept Pulm & Crit Care Med, Beijing, Peoples R China

[2] Chinese Acad Med Sci, Inst Resp Med, Natl Ctr Resp Med, Beijing, Peoples R China

[3] China Japan Friendship Hosp, Inst Clin Med Sci, Beijing, Peoples R China

[4] Peking Univ, Dept Neurosurg, China Japan Friendship Sch Clin Med, Beijing, Peoples R China

[5] China Japan Friendship Hosp, Dept Neurosurg, Beijing, Peoples R China

[6] China Japan Friendship Hosp, Dept Cardiovasc Surg, Beijing, Peoples R China

[7] Harbin Med Univ, Harbin, Heilongjiang, Peoples R China

[8] Tianjin Chest Hosp, Dept Resp & Crit Care Med, 261 Taierzhuang South Rd, Tianjin, Peoples R China

[9] Chinese Acad Med Sci & Peking Union Med Coll, Grad Sch Peking Union Med Coll, Beijing, Peoples R China

[10] Beijing Univ Chem Technol, Coll Life Sci & Technol, Beijing Key Lab Bioproc, Beijing, Peoples R China

[11] Capital Med Univ, Dept Resp Med, Beijing, Peoples R China

[12] Tsinghua Univ Peking Univ Joint Ctr Life Sci, Beijing, Peoples R China

来源：

ISCIENCE | 2022年 / 25卷 / 01期

基金：

国家重点研发计划;

关键词：

SPIKE PROTEIN; VIRUS-INFECTION; ENHANCEMENT; ANTIBODIES; CAPACITY; CELLS; CD4;

D O I：

10.1016/j.isci.2021.103720

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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 Fc gamma RIIA/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 anti-bodies, 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 Fc gamma R-mediated enhanced entry of SARS-CoV-2.

引用

页数：20

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