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2020 ; 134
(12
): 1301-1304
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Decoy ACE2-expressing extracellular vesicles that competitively bind SARS-CoV-2
as a possible COVID-19 therapy
#MMPMID32542396
Inal JM
Clin Sci (Lond)
2020[Jun]; 134
(12
): 1301-1304
PMID32542396
show ga
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.