About: “Amantadine disrupts lysosomal gene expression; potential therapy for COVID19”

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About: “Amantadine disrupts lysosomal gene expression; potential therapy for COVID19” Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	“Amantadine disrupts lysosomal gene expression; potential therapy for COVID19”
Creator	Polymeropoulos, Mihael Przychodzen, Bart Smieszek, Sandra
source	BioRxiv
abstract	SARS-coronavirus 2 is the causal agent of the COVID-19 outbreak. SARS-Cov-2 entry into a cell is dependent upon binding of the viral spike (S) protein to cellular receptor and on cleavage of the spike protein by the host cell proteases such as Cathepsin L and Cathepsin B. CTSL/B are crucial elements of lysosomal pathway and both enzymes are almost exclusively located in the lysosomes.CTSL disruption offers potential for CoVID-19 therapies. The mechanisms of disruption include: decreasing expression of CTSL, direct inhibition of CTSL activity and affecting the conditions of CTSL environment (increase pH in lysosomes). We have conducted a high throughput drug screen gene expression analysis to identify compounds that would downregulate the expression of CTSL/CTSB. One of the top significant results shown to downregulate the expression of the CTSL gene is Amantadine. Amantadine was approved by the US Food and Drug Administration in 1968 as a prophylactic agent for influenza and later for Parkinson’s disease. It is available as a generic drug.. Amantadine in addition to downregulating CTSL appears to further disrupt lysosomal pathway, hence interfering with the capacity of the virus to replicate. It acts as a lysosomotropic agent altering the CTSL functional environment. We hypothesize that Amantadine could decrease the viral load in SARS-CoV-2 positive patients and as such it may serve as a potent therapeutic decreasing the replication and infectivity of the virus likely leading to better clinical outcomes. Clinical studies will be needed to examine the therapeutic utility of amantadine in COVID-19 infection.
has issue date	2020-04-05(xsd:dateTime)
bibo:doi	10.1101/2020.04.05.026187
has license	biorxiv
sha1sum (hex)	4e3f17680dc66471a7fbbccf516b61659c0f0cf6
schema:url	https://doi.org/10.1101/2020.04.05.026187
resource representing a document's title	“Amantadine disrupts lysosomal gene expression; potential therapy for COVID19”
schema:publication	bioRxiv
resource representing a document's body	covid:4e3f17680dc66471a7fbbccf516b61659c0f0cf6#body_text
is schema:about of	named entity 'cell' named entity 'causal' named entity 'potential' named entity 'host' named entity 'dependent' »more»

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