期刊
JOURNAL OF MEDICAL VIROLOGY
卷 94, 期 7, 页码 3251-3256出版社
WILEY
DOI: 10.1002/jmv.27673
关键词
coronavirus; local infection; replication; spread pathogenesis; zoonoses
类别
资金
- National Natural Science Foundation of China
- Sichuan Province Fund for Distinguished Young Scholars
This study discovered that pretreatment with Type I interferon (IFN-I) can effectively block the entry of swine acute diarrhea syndrome coronavirus (SADS-CoV) into cells. The inhibition of SADS-CoV entry and replication mediated by IFN-I is significantly impaired in the absence of TET2. This finding suggests that TET2 serves as a checkpoint for IFN-I-mediated inhibition on the cell entry of SADS-CoV, providing a potential therapeutic target for combating SADS-CoV.
Swine acute diarrhea syndrome coronavirus (SADS-CoV) is a newly discovered bat-origin coronavirus with fatal pathogenicity for neonatal piglets. There is no vaccine to prevent SADS-CoV infection or clinically approved drugs targeting SADS-CoV. Therefore, unraveling cellular factors that regulate SADS-CoV for cell entry is critical to understanding the viral transmission mechanism and provides a potential therapeutic target for SADS-CoV cure. Here, we showed that Type I interferon (IFN-I) pretreatment potently blocks SADS-CoV entry into cells using lentiviral pseudo-virions as targets whose entry is driven by the SADS-CoV Spike glycoprotein. IFN-I-mediated inhibition of SADS-CoV entry and replication was dramatically impaired in the absence of TET2. These results suggest TET2 is found to serve as a checkpoint of IFN-I-meditated inhibition on the cell entry of SADS-CoV, and our discovery might constitute a novel treatment option to combat against SADS-CoV.
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