Potential COVID-19 therapeutics from a rare disease: weaponizing lipid dysregulation to combat viral infectivity.
Identifieur interne : 000E42 ( Main/Exploration ); précédent : 000E41; suivant : 000E43Potential COVID-19 therapeutics from a rare disease: weaponizing lipid dysregulation to combat viral infectivity.
Auteurs : Stephen L. Sturley [États-Unis] ; Tamayanthi Rajakumar [Nouvelle-Zélande] ; Natalie Hammond [Nouvelle-Zélande] ; Katsumi Higaki [Japon] ; Zsuzsa Márka [États-Unis] ; Szabolcs Márka [États-Unis] ; Andrew B. Munkacsi [Nouvelle-Zélande]Source :
- Journal of lipid research [ 1539-7262 ] ; 2020.
Descripteurs français
- KwdFr :
- Androstènes (usage thérapeutique), Anticholestérolémiants (usage thérapeutique), Antiviraux (usage thérapeutique), Betacoronavirus (effets des médicaments et des substances chimiques), Betacoronavirus (métabolisme), Betacoronavirus (pathogénicité), Cholestérol (métabolisme), Glycoprotéine de spicule des coronavirus (génétique), Glycoprotéine de spicule des coronavirus (métabolisme), Humains (MeSH), Hydroxychloroquine (usage thérapeutique), Infections à coronavirus (diagnostic), Infections à coronavirus (traitement médicamenteux), Infections à coronavirus (épidémiologie), Liaison aux protéines (MeSH), Lysosomes (effets des médicaments et des substances chimiques), Lysosomes (métabolisme), Lysosomes (virologie), Maladie de Niemann-Pick de type C (anatomopathologie), Maladie de Niemann-Pick de type C (génétique), Maladie de Niemann-Pick de type C (métabolisme), Maladie de Niemann-Pick de type C (traitement médicamenteux), Pandémies (MeSH), Peptidyl-Dipeptidase A (génétique), Peptidyl-Dipeptidase A (métabolisme), Pneumopathie virale (diagnostic), Pneumopathie virale (traitement médicamenteux), Pneumopathie virale (épidémiologie), Protéines et peptides de signalisation intracellulaire (antagonistes et inhibiteurs), Protéines et peptides de signalisation intracellulaire (génétique), Protéines et peptides de signalisation intracellulaire (métabolisme), Repositionnement des médicaments (méthodes), Récepteurs viraux (antagonistes et inhibiteurs), Récepteurs viraux (génétique), Récepteurs viraux (métabolisme).
- MESH :
- anatomopathologie : Maladie de Niemann-Pick de type C.
- antagonistes et inhibiteurs : Protéines et peptides de signalisation intracellulaire, Récepteurs viraux.
- diagnostic : Infections à coronavirus, Pneumopathie virale.
- effets des médicaments et des substances chimiques : Betacoronavirus, Lysosomes.
- génétique : Glycoprotéine de spicule des coronavirus, Maladie de Niemann-Pick de type C, Peptidyl-Dipeptidase A, Protéines et peptides de signalisation intracellulaire, Récepteurs viraux.
- métabolisme : Betacoronavirus, Cholestérol, Glycoprotéine de spicule des coronavirus, Lysosomes, Maladie de Niemann-Pick de type C, Peptidyl-Dipeptidase A, Protéines et peptides de signalisation intracellulaire, Récepteurs viraux.
- méthodes : Repositionnement des médicaments.
- pathogénicité : Betacoronavirus.
- traitement médicamenteux : Infections à coronavirus, Maladie de Niemann-Pick de type C, Pneumopathie virale.
- usage thérapeutique : Androstènes, Anticholestérolémiants, Antiviraux, Hydroxychloroquine.
- virologie : Lysosomes.
- épidémiologie : Infections à coronavirus, Pneumopathie virale.
- Humains, Liaison aux protéines, Pandémies.
English descriptors
- KwdEn :
- Androstenes (therapeutic use), Angiotensin-Converting Enzyme 2 (MeSH), Anticholesteremic Agents (therapeutic use), Antiviral Agents (therapeutic use), Betacoronavirus (drug effects), Betacoronavirus (metabolism), Betacoronavirus (pathogenicity), COVID-19 (MeSH), Cholesterol (metabolism), Coronavirus Infections (diagnosis), Coronavirus Infections (drug therapy), Coronavirus Infections (epidemiology), Drug Repositioning (methods), Humans (MeSH), Hydroxychloroquine (therapeutic use), Intracellular Signaling Peptides and Proteins (antagonists & inhibitors), Intracellular Signaling Peptides and Proteins (genetics), Intracellular Signaling Peptides and Proteins (metabolism), Lysosomes (drug effects), Lysosomes (metabolism), Lysosomes (virology), Niemann-Pick Disease, Type C (drug therapy), Niemann-Pick Disease, Type C (genetics), Niemann-Pick Disease, Type C (metabolism), Niemann-Pick Disease, Type C (pathology), Pandemics (MeSH), Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (diagnosis), Pneumonia, Viral (drug therapy), Pneumonia, Viral (epidemiology), Protein Binding (MeSH), Receptors, Virus (antagonists & inhibitors), Receptors, Virus (genetics), Receptors, Virus (metabolism), SARS-CoV-2 (MeSH), Spike Glycoprotein, Coronavirus (genetics), Spike Glycoprotein, Coronavirus (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Intracellular Signaling Peptides and Proteins, Receptors, Virus.
- chemical , genetics : Intracellular Signaling Peptides and Proteins, Peptidyl-Dipeptidase A, Receptors, Virus, Spike Glycoprotein, Coronavirus.
- chemical , metabolism : Cholesterol, Intracellular Signaling Peptides and Proteins, Peptidyl-Dipeptidase A, Receptors, Virus, Spike Glycoprotein, Coronavirus.
- chemical , therapeutic use : Androstenes, Anticholesteremic Agents, Antiviral Agents, Hydroxychloroquine.
- chemical : Angiotensin-Converting Enzyme 2.
- diagnosis : Coronavirus Infections, Pneumonia, Viral.
- drug effects : Betacoronavirus, Lysosomes.
- drug therapy : Coronavirus Infections, Niemann-Pick Disease, Type C, Pneumonia, Viral.
- epidemiology : Coronavirus Infections, Pneumonia, Viral.
- genetics : Niemann-Pick Disease, Type C.
- metabolism : Betacoronavirus, Lysosomes, Niemann-Pick Disease, Type C.
- methods : Drug Repositioning.
- pathogenicity : Betacoronavirus.
- pathology : Niemann-Pick Disease, Type C.
- virology : Lysosomes.
- COVID-19, Humans, Pandemics, Protein Binding, SARS-CoV-2.
Abstract
The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 has resulted in the death of more than 328,000 persons worldwide in the first 5 months of 2020. Herculean efforts to rapidly design and produce vaccines and other antiviral interventions are ongoing. However, newly evolving viral mutations, the prospect of only temporary immunity, and a long path to regulatory approval pose significant challenges and call for a common, readily available, and inexpensive treatment. Strategic drug repurposing combined with rapid testing of established molecular targets could provide a pause in disease progression. SARS-CoV-2 shares extensive structural and functional conservation with SARS-CoV-1, including engagement of the same host cell receptor (angiotensin-converting enzyme 2) localized in cholesterol-rich microdomains. These lipid-enveloped viruses encounter the endosomal/lysosomal host compartment in a critical step of infection and maturation. Niemann-Pick type C (NP-C) disease is a rare monogenic neurodegenerative disease caused by deficient efflux of lipids from the late endosome/lysosome (LE/L). The NP-C disease-causing gene (NPC1) has been strongly associated with viral infection, both as a filovirus receptor (e.g., Ebola) and through LE/L lipid trafficking. This suggests that NPC1 inhibitors or NP-C disease mimetics could serve as anti-SARS-CoV-2 agents. Fortunately, there are such clinically approved molecules that elicit antiviral activity in preclinical studies, without causing NP-C disease. Inhibition of NPC1 may impair viral SARS-CoV-2 infectivity via several lipid-dependent mechanisms, which disturb the microenvironment optimum for viral infectivity. We suggest that known mechanistic information on NPC1 could be utilized to identify existing and future drugs to treat COVID-19.
DOI: 10.1194/jlr.R120000851
PubMed: 32457038
PubMed Central: PMC7328045
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Androstenes (therapeutic use)</term>
<term>Angiotensin-Converting Enzyme 2 (MeSH)</term>
<term>Anticholesteremic Agents (therapeutic use)</term>
<term>Antiviral Agents (therapeutic use)</term>
<term>Betacoronavirus (drug effects)</term>
<term>Betacoronavirus (metabolism)</term>
<term>Betacoronavirus (pathogenicity)</term>
<term>COVID-19 (MeSH)</term>
<term>Cholesterol (metabolism)</term>
<term>Coronavirus Infections (diagnosis)</term>
<term>Coronavirus Infections (drug therapy)</term>
<term>Coronavirus Infections (epidemiology)</term>
<term>Drug Repositioning (methods)</term>
<term>Humans (MeSH)</term>
<term>Hydroxychloroquine (therapeutic use)</term>
<term>Intracellular Signaling Peptides and Proteins (antagonists & inhibitors)</term>
<term>Intracellular Signaling Peptides and Proteins (genetics)</term>
<term>Intracellular Signaling Peptides and Proteins (metabolism)</term>
<term>Lysosomes (drug effects)</term>
<term>Lysosomes (metabolism)</term>
<term>Lysosomes (virology)</term>
<term>Niemann-Pick Disease, Type C (drug therapy)</term>
<term>Niemann-Pick Disease, Type C (genetics)</term>
<term>Niemann-Pick Disease, Type C (metabolism)</term>
<term>Niemann-Pick Disease, Type C (pathology)</term>
<term>Pandemics (MeSH)</term>
<term>Peptidyl-Dipeptidase A (genetics)</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
<term>Pneumonia, Viral (diagnosis)</term>
<term>Pneumonia, Viral (drug therapy)</term>
<term>Pneumonia, Viral (epidemiology)</term>
<term>Protein Binding (MeSH)</term>
<term>Receptors, Virus (antagonists & inhibitors)</term>
<term>Receptors, Virus (genetics)</term>
<term>Receptors, Virus (metabolism)</term>
<term>SARS-CoV-2 (MeSH)</term>
<term>Spike Glycoprotein, Coronavirus (genetics)</term>
<term>Spike Glycoprotein, Coronavirus (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Androstènes (usage thérapeutique)</term>
<term>Anticholestérolémiants (usage thérapeutique)</term>
<term>Antiviraux (usage thérapeutique)</term>
<term>Betacoronavirus (effets des médicaments et des substances chimiques)</term>
<term>Betacoronavirus (métabolisme)</term>
<term>Betacoronavirus (pathogénicité)</term>
<term>Cholestérol (métabolisme)</term>
<term>Glycoprotéine de spicule des coronavirus (génétique)</term>
<term>Glycoprotéine de spicule des coronavirus (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Hydroxychloroquine (usage thérapeutique)</term>
<term>Infections à coronavirus (diagnostic)</term>
<term>Infections à coronavirus (traitement médicamenteux)</term>
<term>Infections à coronavirus (épidémiologie)</term>
<term>Liaison aux protéines (MeSH)</term>
<term>Lysosomes (effets des médicaments et des substances chimiques)</term>
<term>Lysosomes (métabolisme)</term>
<term>Lysosomes (virologie)</term>
<term>Maladie de Niemann-Pick de type C (anatomopathologie)</term>
<term>Maladie de Niemann-Pick de type C (génétique)</term>
<term>Maladie de Niemann-Pick de type C (métabolisme)</term>
<term>Maladie de Niemann-Pick de type C (traitement médicamenteux)</term>
<term>Pandémies (MeSH)</term>
<term>Peptidyl-Dipeptidase A (génétique)</term>
<term>Peptidyl-Dipeptidase A (métabolisme)</term>
<term>Pneumopathie virale (diagnostic)</term>
<term>Pneumopathie virale (traitement médicamenteux)</term>
<term>Pneumopathie virale (épidémiologie)</term>
<term>Protéines et peptides de signalisation intracellulaire (antagonistes et inhibiteurs)</term>
<term>Protéines et peptides de signalisation intracellulaire (génétique)</term>
<term>Protéines et peptides de signalisation intracellulaire (métabolisme)</term>
<term>Repositionnement des médicaments (méthodes)</term>
<term>Récepteurs viraux (antagonistes et inhibiteurs)</term>
<term>Récepteurs viraux (génétique)</term>
<term>Récepteurs viraux (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Intracellular Signaling Peptides and Proteins</term>
<term>Receptors, Virus</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Intracellular Signaling Peptides and Proteins</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Receptors, Virus</term>
<term>Spike Glycoprotein, Coronavirus</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cholesterol</term>
<term>Intracellular Signaling Peptides and Proteins</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Receptors, Virus</term>
<term>Spike Glycoprotein, Coronavirus</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Androstenes</term>
<term>Anticholesteremic Agents</term>
<term>Antiviral Agents</term>
<term>Hydroxychloroquine</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Angiotensin-Converting Enzyme 2</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Maladie de Niemann-Pick de type C</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines et peptides de signalisation intracellulaire</term>
<term>Récepteurs viraux</term>
</keywords>
<keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Coronavirus Infections</term>
<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="diagnostic" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Pneumopathie virale</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Betacoronavirus</term>
<term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronavirus Infections</term>
<term>Niemann-Pick Disease, Type C</term>
<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Betacoronavirus</term>
<term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Coronavirus Infections</term>
<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Niemann-Pick Disease, Type C</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glycoprotéine de spicule des coronavirus</term>
<term>Maladie de Niemann-Pick de type C</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Protéines et peptides de signalisation intracellulaire</term>
<term>Récepteurs viraux</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Betacoronavirus</term>
<term>Lysosomes</term>
<term>Niemann-Pick Disease, Type C</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Drug Repositioning</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Betacoronavirus</term>
<term>Cholestérol</term>
<term>Glycoprotéine de spicule des coronavirus</term>
<term>Lysosomes</term>
<term>Maladie de Niemann-Pick de type C</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Protéines et peptides de signalisation intracellulaire</term>
<term>Récepteurs viraux</term>
</keywords>
<keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Repositionnement des médicaments</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Betacoronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Betacoronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Niemann-Pick Disease, Type C</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Maladie de Niemann-Pick de type C</term>
<term>Pneumopathie virale</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Androstènes</term>
<term>Anticholestérolémiants</term>
<term>Antiviraux</term>
<term>Hydroxychloroquine</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="épidémiologie" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Pneumopathie virale</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>COVID-19</term>
<term>Humans</term>
<term>Pandemics</term>
<term>Protein Binding</term>
<term>SARS-CoV-2</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Liaison aux protéines</term>
<term>Pandémies</term>
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<front><div type="abstract" xml:lang="en">The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 has resulted in the death of more than 328,000 persons worldwide in the first 5 months of 2020. Herculean efforts to rapidly design and produce vaccines and other antiviral interventions are ongoing. However, newly evolving viral mutations, the prospect of only temporary immunity, and a long path to regulatory approval pose significant challenges and call for a common, readily available, and inexpensive treatment. Strategic drug repurposing combined with rapid testing of established molecular targets could provide a pause in disease progression. SARS-CoV-2 shares extensive structural and functional conservation with SARS-CoV-1, including engagement of the same host cell receptor (angiotensin-converting enzyme 2) localized in cholesterol-rich microdomains. These lipid-enveloped viruses encounter the endosomal/lysosomal host compartment in a critical step of infection and maturation. Niemann-Pick type C (NP-C) disease is a rare monogenic neurodegenerative disease caused by deficient efflux of lipids from the late endosome/lysosome (LE/L). The NP-C disease-causing gene (NPC1) has been strongly associated with viral infection, both as a filovirus receptor (e.g., Ebola) and through LE/L lipid trafficking. This suggests that NPC1 inhibitors or NP-C disease mimetics could serve as anti-SARS-CoV-2 agents. Fortunately, there are such clinically approved molecules that elicit antiviral activity in preclinical studies, without causing NP-C disease. Inhibition of NPC1 may impair viral SARS-CoV-2 infectivity via several lipid-dependent mechanisms, which disturb the microenvironment optimum for viral infectivity. We suggest that known mechanistic information on NPC1 could be utilized to identify existing and future drugs to treat COVID-19.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32457038</PMID>
<DateCompleted><Year>2020</Year>
<Month>07</Month>
<Day>14</Day>
</DateCompleted>
<DateRevised><Year>2021</Year>
<Month>03</Month>
<Day>30</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1539-7262</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>61</Volume>
<Issue>7</Issue>
<PubDate><Year>2020</Year>
<Month>07</Month>
</PubDate>
</JournalIssue>
<Title>Journal of lipid research</Title>
<ISOAbbreviation>J Lipid Res</ISOAbbreviation>
</Journal>
<ArticleTitle>Potential COVID-19 therapeutics from a rare disease: weaponizing lipid dysregulation to combat viral infectivity.</ArticleTitle>
<Pagination><MedlinePgn>972-982</MedlinePgn>
</Pagination>
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<ELocationID EIdType="doi" ValidYN="Y">10.1194/jlr.R120000851</ELocationID>
<Abstract><AbstractText>The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 has resulted in the death of more than 328,000 persons worldwide in the first 5 months of 2020. Herculean efforts to rapidly design and produce vaccines and other antiviral interventions are ongoing. However, newly evolving viral mutations, the prospect of only temporary immunity, and a long path to regulatory approval pose significant challenges and call for a common, readily available, and inexpensive treatment. Strategic drug repurposing combined with rapid testing of established molecular targets could provide a pause in disease progression. SARS-CoV-2 shares extensive structural and functional conservation with SARS-CoV-1, including engagement of the same host cell receptor (angiotensin-converting enzyme 2) localized in cholesterol-rich microdomains. These lipid-enveloped viruses encounter the endosomal/lysosomal host compartment in a critical step of infection and maturation. Niemann-Pick type C (NP-C) disease is a rare monogenic neurodegenerative disease caused by deficient efflux of lipids from the late endosome/lysosome (LE/L). The NP-C disease-causing gene (NPC1) has been strongly associated with viral infection, both as a filovirus receptor (e.g., Ebola) and through LE/L lipid trafficking. This suggests that NPC1 inhibitors or NP-C disease mimetics could serve as anti-SARS-CoV-2 agents. Fortunately, there are such clinically approved molecules that elicit antiviral activity in preclinical studies, without causing NP-C disease. Inhibition of NPC1 may impair viral SARS-CoV-2 infectivity via several lipid-dependent mechanisms, which disturb the microenvironment optimum for viral infectivity. We suggest that known mechanistic information on NPC1 could be utilized to identify existing and future drugs to treat COVID-19.</AbstractText>
<CopyrightInformation>Copyright © 2020 Sturley et al.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sturley</LastName>
<ForeName>Stephen L</ForeName>
<Initials>SL</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Barnard College, New York, NY 10027. Electronic address: mailto:sls37@columbia.edu.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rajakumar</LastName>
<ForeName>Tamayanthi</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>School of Biological Sciences and Centre for Biodiscovery, Victoria University of Wellington, Wellington 6012, New Zealand.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hammond</LastName>
<ForeName>Natalie</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>School of Biological Sciences and Centre for Biodiscovery, Victoria University of Wellington, Wellington 6012, New Zealand.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Higaki</LastName>
<ForeName>Katsumi</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Division of Functional Genomics, Tottori University, Yonago 683-8503, Japan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Márka</LastName>
<ForeName>Zsuzsa</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Physics, Columbia University, New York, NY 10027.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Márka</LastName>
<ForeName>Szabolcs</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Physics, Columbia University, New York, NY 10027.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Munkacsi</LastName>
<ForeName>Andrew B</ForeName>
<Initials>AB</Initials>
<AffiliationInfo><Affiliation>School of Biological Sciences and Centre for Biodiscovery, Victoria University of Wellington, Wellington 6012, New Zealand.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 DK054320</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 HL007343</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM129465</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D016454">Review</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>05</Month>
<Day>26</Day>
</ArticleDate>
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<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>J Lipid Res</MedlineTA>
<NlmUniqueID>0376606</NlmUniqueID>
<ISSNLinking>0022-2275</ISSNLinking>
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<NameOfSubstance UI="C106881">NPC1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D011991">Receptors, Virus</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D064370">Spike Glycoprotein, Coronavirus</NameOfSubstance>
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<Chemical><RegistryNumber>3039-71-2</RegistryNumber>
<NameOfSubstance UI="C006261">3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one</NameOfSubstance>
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<NameOfSubstance UI="D007703">Peptidyl-Dipeptidase A</NameOfSubstance>
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<NameOfSubstance UI="C000705307">ACE2 protein, human</NameOfSubstance>
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<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="N">Betacoronavirus</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="N">COVID-19</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002784" MajorTopicYN="N">Cholesterol</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName>
<QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058492" MajorTopicYN="N">Drug Repositioning</DescriptorName>
<QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006886" MajorTopicYN="N">Hydroxychloroquine</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047908" MajorTopicYN="N">Intracellular Signaling Peptides and Proteins</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D052556" MajorTopicYN="N">Niemann-Pick Disease, Type C</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D058873" MajorTopicYN="Y">Pandemics</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName>
<QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011991" MajorTopicYN="N">Receptors, Virus</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064370" MajorTopicYN="N">Spike Glycoprotein, Coronavirus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Ebola</Keyword>
<Keyword MajorTopicYN="Y">Niemann-Pick disease</Keyword>
<Keyword MajorTopicYN="Y">cholesterol</Keyword>
<Keyword MajorTopicYN="Y">cholesterol trafficking</Keyword>
<Keyword MajorTopicYN="Y">coronavirus disease 2019</Keyword>
<Keyword MajorTopicYN="Y">drug repurposing</Keyword>
<Keyword MajorTopicYN="Y">dyslipidemias</Keyword>
<Keyword MajorTopicYN="Y">lysosomal storage disease</Keyword>
<Keyword MajorTopicYN="Y">pandemic</Keyword>
<Keyword MajorTopicYN="Y">severe acute respiratory syndrome coronavirus 2</Keyword>
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