Signal Transduct Target Ther
. 2021 May 12;6(1):189.
doi: 10.1038/s41392-021-00604-5.
The interferon-stimulated exosomal hACE2 potently inhibits SARS-CoV-2 replication through competitively blocking the virus entry
Junsong Zhang # 1 2 , Feng Huang # 2 3 , Baijin Xia 2 , Yaochang Yuan 2 , Fei Yu 1 2 , Guanwen Wang 1 , Qianyu Chen 1 , Qian Wang 1 , Yuzhuang Li 2 , Rong Li 2 , Zheng Song 2 , Ting Pan 2 4 , Jingliang Chen 2 5 , Gen Lu 6 , Hui Zhang 7
Affiliations
- PMID: 33980808
- DOI: 10.1038/s41392-021-00604-5
Abstract
Since the outbreak of coronavirus disease 2019 (COVID-19), it has become a global pandemic. The spike (S) protein of etiologic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) specifically recognizes human angiotensin-converting enzyme 2 (hACE2) as its receptor, which is recently identified as an interferon (IFN)-stimulated gene. Here, we find that hACE2 exists on the surface of exosomes released by different cell types, and the expression of exosomal hACE2 is increased by IFN?/? treatment. In particular, exosomal hACE2 can specifically block the cell entry of SARS-CoV-2, subsequently inhibit the replication of SARS-CoV-2 in vitro and ex vivo. Our findings have indicated that IFN is able to upregulate a viral receptor on the exosomes which competitively block the virus entry, exhibiting a potential antiviral strategy.