Decoy ACE2-expressing extracellular vesicles that competitively bind SARS-CoV-2 as a possible COVID-19 therapy

Jameel M. Inal

doi:10.1042/CS20200623

Decoy ACE2-expressing extracellular vesicles that competitively bind SARS-CoV-2 as a possible COVID-19 therapy

Jameel M. Inal

Biosciences Research Group

Research output: Contribution to journal › Comment/debate › peer-review

35 Citations (Scopus)

38 Downloads (Pure)

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.

Original language	English
Pages (from-to)	1301-1304
Number of pages	4
Journal	Clinical science (London, England : 1979)
Volume	134
Issue number	12
DOIs	https://doi.org/10.1042/CS20200623
Publication status	Published - 16 Jun 2020

Keywords

ARDS
competitive inhibition therapy
COVID-19
Extracellular Vesicles
SARS-CoV-2
Coronavirus Infections
Pandemics
Humans
Angiotensins
Peptidyl-Dipeptidase A
SARS Virus
Betacoronavirus
Pneumonia, Viral

Access to Document

10.1042/CS20200623Licence: CC BY-NC-ND

Final_Version
© 2020 The Author(s). This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY-NC-ND - https://creativecommons.org/licenses/by-nc-nd/4.0/).
Final published version, 453 KBLicence: CC BY-NC-ND

Cite this

@article{7e553546db554d7c87abc786b59c43c4,

title = "Decoy ACE2-expressing extracellular vesicles that competitively bind SARS-CoV-2 as a possible COVID-19 therapy",

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, competitive inhibition therapy, COVID-19, Extracellular Vesicles, SARS-CoV-2, Coronavirus Infections, Pandemics, Humans, Angiotensins, Peptidyl-Dipeptidase A, SARS Virus, Betacoronavirus, Pneumonia, Viral",

author = "Inal, {Jameel M.}",

note = "{\textcopyright} 2020 The Author(s). This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY-NC-ND - https://creativecommons.org/licenses/by-nc-nd/4.0/).",

year = "2020",

month = jun,

day = "16",

doi = "10.1042/CS20200623",

language = "English",

volume = "134",

pages = "1301--1304",

journal = "Clinical science (London, England : 1979)",

issn = "0143-5221",

publisher = "Portland Press Ltd.",

number = "12",

}

TY - JOUR

T1 - Decoy ACE2-expressing extracellular vesicles that competitively bind SARS-CoV-2 as a possible COVID-19 therapy

AU - Inal, Jameel M.

N1 - © 2020 The Author(s). This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY-NC-ND - https://creativecommons.org/licenses/by-nc-nd/4.0/).

PY - 2020/6/16

Y1 - 2020/6/16

N2 - 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.

AB - 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.

KW - ARDS

KW - competitive inhibition therapy

KW - COVID-19

KW - Extracellular Vesicles

KW - SARS-CoV-2

KW - Coronavirus Infections

KW - Pandemics

KW - Humans

KW - Angiotensins

KW - Peptidyl-Dipeptidase A

KW - SARS Virus

KW - Betacoronavirus

KW - Pneumonia, Viral

UR - http://www.scopus.com/inward/record.url?scp=85086625666&partnerID=8YFLogxK

U2 - 10.1042/CS20200623

DO - 10.1042/CS20200623

M3 - Comment/debate

C2 - 32542396

AN - SCOPUS:85086625666

SN - 0143-5221

VL - 134

SP - 1301

EP - 1304

JO - Clinical science (London, England : 1979)

JF - Clinical science (London, England : 1979)

IS - 12

ER -

Decoy ACE2-expressing extracellular vesicles that competitively bind SARS-CoV-2 as a possible COVID-19 therapy

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this