ACE2 Shedding and Furin Abundance in Target Organs may Influence the Efficiency of SARS-CoV-2 Entry
Yuanchen Ma1, #, Yinong Huang1, 2, #, Tao Wang1, Andy Peng Xiang1, Weijun Huang1, *
Identifiers and Pagination:Year: 2021
First Page: 1
Last Page: 12
Publisher Id: TOBIOIJ-14-1
Article History:Received Date: 29/8/2020
Revision Received Date: 11/1/2021
Acceptance Date: 13/1/2021
Electronic publication date: 22/03/2021
Collection year: 2021
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a lineage B coronavirus, causing the worldwide outbreak of Corona Virus Disease 2019 (COVID-19). Despite genetically closed to SARS-CoV, SARS-CoV-2 seems to possess enhanced infectivity and subtle different clinical features, which may hamper the early screening of suspected patients as well as the control of virus transmission. Unfortunately, there are few tools to predict the potential target organ damage and possible clinical manifestations caused by such novel coronavirus.
To solve this problem, we use the online single-cell sequence datasets to analyze the expression of the major receptor in host cells that mediates the virus entry, including angiotensin converting enzyme 2 (ACE2), and its co-expressed membrane endopeptidases.
The results indicated the differential expression of ADAM10 and ADAM17 might contribute to the ACE2 shedding and affect the membrane ACE2 abundance. We further confirm a putative furin-cleavage site reported recently in the spike protein of SARS-CoV-2, which may facilitate the virus-cell fusion. Based on these findings, we develop an approach that comprehensively analyzed the virus receptor expression, ACE2 shedding, membrane fusion activity, virus uptake and virus replication to evaluate the infectivity of SARS-CoV-2 to different human organs.
Our results indicate that, in addition to airway epithelia, cardiac tissue and enteric canals are susceptible to SARS-CoV-2 as well.