tetano
Editor, Senior Moderator
Clin Sci (Lond)
. 2020 Jun 26;134(12):1301-1304.
doi: 10.1042/CS20200623.
Decoy ACE2-expressing Extracellular Vesicles That Competitively Bind SARS-CoV-2 as a Possible COVID-19 Therapy
Jameel M Inal[SUP] 1 2 [/SUP]
Affiliations
Abstract
The novel strain of coronavirus that appeared in 2019, SARS-CoV-2, is the causative agent of severe respiratory disease, COVID-19, and the ongoing pandemic. As for SARS-CoV that caused the SARS 2003 epidemic, the receptor on host cells that promotes uptake, through attachment of the spike (S) protein of the virus, is angiotensin-converting enzyme 2 (ACE2). In a recent article published by Batlle et al. (Clin. Sci. (Lond.) (2020) 134, 543-545) it was suggested that soluble recombinant ACE2 could be used as a novel biological therapeutic to intercept the virus, limiting the progression of infection and reducing lung injury. Another way, discussed here, to capture SARS-CoV-2, as an adjunct or alternative, would be to use ACE2+-small extracellular vesicles (sEVs). A competitive inhibition therapy could therefore be developed, using sEVs from engineered mesenchymal stromal/stem cells (MSCs), overexpressing ACE2.
Keywords: ARDS; COVID-19; Extracellular Vesicles; SARS-CoV-2; competitive inhibition therapy.
. 2020 Jun 26;134(12):1301-1304.
doi: 10.1042/CS20200623.
Decoy ACE2-expressing Extracellular Vesicles That Competitively Bind SARS-CoV-2 as a Possible COVID-19 Therapy
Jameel M Inal[SUP] 1 2 [/SUP]
Affiliations
- PMID: 32542396
- DOI: 10.1042/CS20200623
Abstract
The novel strain of coronavirus that appeared in 2019, SARS-CoV-2, is the causative agent of severe respiratory disease, COVID-19, and the ongoing pandemic. As for SARS-CoV that caused the SARS 2003 epidemic, the receptor on host cells that promotes uptake, through attachment of the spike (S) protein of the virus, is angiotensin-converting enzyme 2 (ACE2). In a recent article published by Batlle et al. (Clin. Sci. (Lond.) (2020) 134, 543-545) it was suggested that soluble recombinant ACE2 could be used as a novel biological therapeutic to intercept the virus, limiting the progression of infection and reducing lung injury. Another way, discussed here, to capture SARS-CoV-2, as an adjunct or alternative, would be to use ACE2+-small extracellular vesicles (sEVs). A competitive inhibition therapy could therefore be developed, using sEVs from engineered mesenchymal stromal/stem cells (MSCs), overexpressing ACE2.
Keywords: ARDS; COVID-19; Extracellular Vesicles; SARS-CoV-2; competitive inhibition therapy.