CovidChloroV1, Main, Corpus, bibRecord, 000E50

Hydroxychloroquine: mechanism of action inhibiting SARS-CoV2 entry.

Identifieur interne : 000E50 ( Main/Corpus ); précédent : 000E49; suivant : 000E51

Hydroxychloroquine: mechanism of action inhibiting SARS-CoV2 entry.

Auteurs : Zixuan Yuan ; Mahmud Arif Pavel ; Hao Wang ; Scott B. Hansen

Source :

bioRxiv : the preprint server for biology ; 2020.

RBID : pubmed:32817933

Abstract

Background

SARS-coronavirus 2 (SARS-CoV-2) is currently causing a worldwide pandemic. Potential drugs identified for the treatment of SARS-CoV-2 infection include chloroquine (CQ), its derivative hydroxychloroquine (HCQ), and the anesthetic propofol. Their mechanism of action in SARS-CoV-2 infection is poorly understood. Recently, anesthetics, both general and local, were shown to disrupt ordered lipid domains. These same lipid domains recruit the SARS-CoV-2 surface receptor angiotensin converting enzyme 2 (ACE2) to an endocytic entry point and their disruption by cholesterol depletion decreases ACE2 recruitment and viral entry.

Methods

Viral entry was determined using a SARS-CoV-2 pseudovirus (SARS2-PV) and a luciferase reporter gene expressed by the virus after treatment of the cells with 50 μM propofol, tetracaine, HCQ, and erythromycin. HCQ disruption of monosialotetrahexosylganglioside1 (GM1) lipid rafts, phosphatidylinositol 4,5-bisphosphate (PIP

Results

Propofol, tetracaine, and HCQ inhibit SARS2-PV viral entry. HCQ directly perturbs both GM1 lipid rafts and PIP

Conclusions

We conclude HCQ is an anesthetic-like compound that disrupts GM1 lipid rafts similar to propofol and other local or general anesthetics. Furthermore, we conclude disruption of GM1 raft function, and not the concentration of GM1 raft molecules, governs the antiviral properties of HCQ. HCQ disruption of the membrane appears to also disrupt the production of host defense peptide, hence an antimicrobial such as erythromycin could be an important combined treatment. Nonetheless erythromycin has anti-SARS-CoV-2 activity and may combine with HCQ to reduce infection.

KEY POINTS

DOI: 10.1101/2020.08.13.250217
PubMed: 32817933
PubMed Central: PMC7430563

Links to Exploration step

pubmed:32817933

Le document en format XML

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<author><name sortKey="Yuan, Zixuan" sort="Yuan, Zixuan" uniqKey="Yuan Z" first="Zixuan" last="Yuan">Zixuan Yuan</name>
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<author><name sortKey="Pavel, Mahmud Arif" sort="Pavel, Mahmud Arif" uniqKey="Pavel M" first="Mahmud Arif" last="Pavel">Mahmud Arif Pavel</name>
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<author><name sortKey="Wang, Hao" sort="Wang, Hao" uniqKey="Wang H" first="Hao" last="Wang">Hao Wang</name>
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<author><name sortKey="Hansen, Scott B" sort="Hansen, Scott B" uniqKey="Hansen S" first="Scott B" last="Hansen">Scott B. Hansen</name>
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<front><div type="abstract" xml:lang="en"><p><b>Background</b>
</p>
<p>SARS-coronavirus 2 (SARS-CoV-2) is currently causing a worldwide pandemic. Potential drugs identified for the treatment of SARS-CoV-2 infection include chloroquine (CQ), its derivative hydroxychloroquine (HCQ), and the anesthetic propofol. Their mechanism of action in SARS-CoV-2 infection is poorly understood. Recently, anesthetics, both general and local, were shown to disrupt ordered lipid domains. These same lipid domains recruit the SARS-CoV-2 surface receptor angiotensin converting enzyme 2 (ACE2) to an endocytic entry point and their disruption by cholesterol depletion decreases ACE2 recruitment and viral entry.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>Methods</b>
</p>
<p>Viral entry was determined using a SARS-CoV-2 pseudovirus (SARS2-PV) and a luciferase reporter gene expressed by the virus after treatment of the cells with 50 μM propofol, tetracaine, HCQ, and erythromycin. HCQ disruption of monosialotetrahexosylganglioside1 (GM1) lipid rafts, phosphatidylinositol 4,5-bisphosphate (PIP </p>
</div>
<div type="abstract" xml:lang="en"><p><b>Results</b>
</p>
<p>Propofol, tetracaine, and HCQ inhibit SARS2-PV viral entry. HCQ directly perturbs both GM1 lipid rafts and PIP </p>
</div>
<div type="abstract" xml:lang="en"><p><b>Conclusions</b>
</p>
<p>We conclude HCQ is an anesthetic-like compound that disrupts GM1 lipid rafts similar to propofol and other local or general anesthetics. Furthermore, we conclude disruption of GM1 raft function, and not the concentration of GM1 raft molecules, governs the antiviral properties of HCQ. HCQ disruption of the membrane appears to also disrupt the production of host defense peptide, hence an antimicrobial such as erythromycin could be an important combined treatment. Nonetheless erythromycin has anti-SARS-CoV-2 activity and may combine with HCQ to reduce infection.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>KEY POINTS</b>
</p>
<p></p>
</div>
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<ArticleTitle>Hydroxychloroquine: mechanism of action inhibiting SARS-CoV2 entry.</ArticleTitle>
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<Abstract><AbstractText Label="Background" NlmCategory="UNASSIGNED">SARS-coronavirus 2 (SARS-CoV-2) is currently causing a worldwide pandemic. Potential drugs identified for the treatment of SARS-CoV-2 infection include chloroquine (CQ), its derivative hydroxychloroquine (HCQ), and the anesthetic propofol. Their mechanism of action in SARS-CoV-2 infection is poorly understood. Recently, anesthetics, both general and local, were shown to disrupt ordered lipid domains. These same lipid domains recruit the SARS-CoV-2 surface receptor angiotensin converting enzyme 2 (ACE2) to an endocytic entry point and their disruption by cholesterol depletion decreases ACE2 recruitment and viral entry.</AbstractText>
<AbstractText Label="Methods" NlmCategory="UNASSIGNED">Viral entry was determined using a SARS-CoV-2 pseudovirus (SARS2-PV) and a luciferase reporter gene expressed by the virus after treatment of the cells with 50 μM propofol, tetracaine, HCQ, and erythromycin. HCQ disruption of monosialotetrahexosylganglioside1 (GM1) lipid rafts, phosphatidylinositol 4,5-bisphosphate (PIP <sub>2</sub>
 ) domains, and ACE2 receptor at nanoscale distances was monitored by direct stochastic reconstruction microscopy (dSTORM). Cells were fixed, permeabilized, and then labeled with either fluorescent cholera toxin B (CTxB) or antibody and then fixed again prior to imaging. Cluster analysis of dSTORM images was used to determine size and number and cross pair correlation was used to determine trafficking of endogenously expressed ACE2 in and out of lipid domains.</AbstractText>
<AbstractText Label="Results" NlmCategory="UNASSIGNED">Propofol, tetracaine, and HCQ inhibit SARS2-PV viral entry. HCQ directly perturbs both GM1 lipid rafts and PIP <sub>2</sub>
 domains. GM1 rafts increased in size and number similar to anesthetic disruption of lipid rafts; PIP <sub>2</sub>
 domains decreased in size and number. HCQ blocked both GM1 and PIP <sub>2</sub>
 domains ability to attract and cluster ACE2.</AbstractText>
<AbstractText Label="Conclusions" NlmCategory="UNASSIGNED">We conclude HCQ is an anesthetic-like compound that disrupts GM1 lipid rafts similar to propofol and other local or general anesthetics. Furthermore, we conclude disruption of GM1 raft function, and not the concentration of GM1 raft molecules, governs the antiviral properties of HCQ. HCQ disruption of the membrane appears to also disrupt the production of host defense peptide, hence an antimicrobial such as erythromycin could be an important combined treatment. Nonetheless erythromycin has anti-SARS-CoV-2 activity and may combine with HCQ to reduce infection.</AbstractText>
<AbstractText Label="KEY POINTS" NlmCategory="CONCLUSIONS"><i>Question:</i>
 What is the molecular basis for antiviral activity of hydroxychloroquine and propofol? <i>Findings:</i>
 Hydroxychloroquine disrupt lipid rafts similar to local and general anesthetics. <i>Meaning:</i>
 Since lipids cluster ACE2 and facilitate viral entry, hydroxychloroquine and anesthetics appear to inhibit viral entry by disrupting the lipid clustering and ACE2 localization.</AbstractText>
</Abstract>
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Hydroxychloroquine: mechanism of action inhibiting SARS-CoV2 entry.

Hydroxychloroquine: mechanism of action inhibiting SARS-CoV2 entry.

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