期刊
NATURE GENETICS
卷 53, 期 2, 页码 205-+出版社
NATURE RESEARCH
DOI: 10.1038/s41588-020-00759-x
关键词
-
资金
- Asthma, Allergy and Inflammation Research (AAIR) Charity [AAIR/01/ACE2/2020]
- National Institute for Health Research (NIHR) Southampton Biomedical Research Centre (BRC)
- NIHR Wellcome Trust
- AAIR [AAIR/hybrid_cilia/2020]
- Wellcome Trust Seed Award in Science [204378/Z/16/Z]
- NIHR Research Professorship [RP-2016-07-011]
- NHS England PCD National Service
- Medical Research Foundation [MRF-091-0003-RG-CONFO]
- European Respiratory Society
- AAIR Charity Research Grant
- NIHR Southampton BRC
- Medical Research Foundation [MRF-091-0003-RG-CONFO] Funding Source: researchfish
- BBSRC [BB/P011365/1] Funding Source: UKRI
A novel short isoform of ACE2, substantially upregulated in response to interferon stimulation and rhinovirus infection, was identified in airway epithelial cells, the main site of SARS-CoV-2 infection. This short isoform lacks high-affinity binding sites for the SARS-CoV-2 spike protein, suggesting it may not directly contribute to host susceptibility to SARS-CoV-2 infection.
Angiotensin-converting enzyme 2 (ACE2) is the main entry point in airway epithelial cells for SARS-CoV-2. ACE2 binding to the SARS-CoV-2 protein spike triggers viral fusion with the cell plasma membrane, resulting in viral RNA genome delivery into the host. Despite ACE2's critical role in SARS-CoV-2 infection, full understanding of ACE2 expression, including in response to viral infection, remains unclear. ACE2 was thought to encode five transcripts and one protein of 805 amino acids. In the present study, we identify a novel short isoform of ACE2 expressed in the airway epithelium, the main site of SARS-CoV-2 infection. Short ACE2 is substantially upregulated in response to interferon stimulation and rhinovirus infection, but not SARS-CoV-2 infection. This short isoform lacks SARS-CoV-2 spike high-affinity binding sites and, altogether, our data are consistent with a model where short ACE2 is unlikely to directly contribute to host susceptibility to SARS-CoV-2 infection.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据