tetano
Editor, Senior Moderator
Med Virol
. 2020 Jun 4.
doi: 10.1002/jmv.26139. Online ahead of print.
Increasing Host Cellular Receptor-Angiotensin-Converting Enzyme 2 (ACE2) Expression by Coronavirus May Facilitate 2019-nCoV (Or SARS-CoV-2) Infection
Meng-Wei Zhuang[SUP] 1 [/SUP], Yun Cheng[SUP] 2 [/SUP], Jing Zhang[SUP] 1 [/SUP], Xue-Mei Jiang[SUP] 3 [/SUP], Li Wang[SUP] 3 [/SUP], Jian Deng[SUP] 2 [/SUP], Pei-Hui Wang[SUP] 1 [/SUP]
Affiliations
Abstract
The ongoing outbreak of a new coronavirus (2019-nCoV, or SARS-CoV-2) has caused an epidemic of the acute respiratory syndrome known as COVID-19 in humans. SARS-CoV-2 rapidly spread to multiple regions of China and multiple other countries, posing a serious threat to public health. The spike (S) proteins of SARS-CoV-1 and SARS-CoV-2 may use the same host cellular receptor, angiotensin-converting enzyme 2 (ACE2), for entering into host cells. The affinity between ACE2 and the SARS-CoV-2 S protein is much higher than that of ACE2 binding to the SARS-CoV S protein, explaining why SARS-CoV-2 seems to be more readily transmitted from the human to human. Here, we report that ACE2 can be significantly upregulated after infection of various viruses, including SARS-CoV-1 and SARS-CoV-2, or by the stimulation with inflammatory cytokines such as interferons. We propose that SARS-CoV-2 may positively induce its cellular entry receptor, ACE2, to accelerate its replication and spread; high inflammatory cytokine levels increase ACE2 expression and act as high-risk factors for developing COVID-19, and the infection of other viruses may increase the risk of SARS-CoV-2 infection. Therefore, drugs targeting ACE2 may be developed for the future emerging infectious diseases caused by this cluster of coronaviruses. This article is protected by copyright. All rights reserved.
Keywords: 2019-nCoV; ACE2; COVID-19; IFN; ISG; SARS-CoV-2.
. 2020 Jun 4.
doi: 10.1002/jmv.26139. Online ahead of print.
Increasing Host Cellular Receptor-Angiotensin-Converting Enzyme 2 (ACE2) Expression by Coronavirus May Facilitate 2019-nCoV (Or SARS-CoV-2) Infection
Meng-Wei Zhuang[SUP] 1 [/SUP], Yun Cheng[SUP] 2 [/SUP], Jing Zhang[SUP] 1 [/SUP], Xue-Mei Jiang[SUP] 3 [/SUP], Li Wang[SUP] 3 [/SUP], Jian Deng[SUP] 2 [/SUP], Pei-Hui Wang[SUP] 1 [/SUP]
Affiliations
- PMID: 32497323
- DOI: 10.1002/jmv.26139
Abstract
The ongoing outbreak of a new coronavirus (2019-nCoV, or SARS-CoV-2) has caused an epidemic of the acute respiratory syndrome known as COVID-19 in humans. SARS-CoV-2 rapidly spread to multiple regions of China and multiple other countries, posing a serious threat to public health. The spike (S) proteins of SARS-CoV-1 and SARS-CoV-2 may use the same host cellular receptor, angiotensin-converting enzyme 2 (ACE2), for entering into host cells. The affinity between ACE2 and the SARS-CoV-2 S protein is much higher than that of ACE2 binding to the SARS-CoV S protein, explaining why SARS-CoV-2 seems to be more readily transmitted from the human to human. Here, we report that ACE2 can be significantly upregulated after infection of various viruses, including SARS-CoV-1 and SARS-CoV-2, or by the stimulation with inflammatory cytokines such as interferons. We propose that SARS-CoV-2 may positively induce its cellular entry receptor, ACE2, to accelerate its replication and spread; high inflammatory cytokine levels increase ACE2 expression and act as high-risk factors for developing COVID-19, and the infection of other viruses may increase the risk of SARS-CoV-2 infection. Therefore, drugs targeting ACE2 may be developed for the future emerging infectious diseases caused by this cluster of coronaviruses. This article is protected by copyright. All rights reserved.
Keywords: 2019-nCoV; ACE2; COVID-19; IFN; ISG; SARS-CoV-2.