Potential COVID-19 therapeutics from a rare disease: weaponizing lipid dysregulation to combat viral infectivity.
Identifieur interne : 001581 ( Main/Corpus ); précédent : 001580; suivant : 001582Potential COVID-19 therapeutics from a rare disease: weaponizing lipid dysregulation to combat viral infectivity.
Auteurs : Stephen L. Sturley ; Tamayanthi Rajakumar ; Natalie Hammond ; Katsumi Higaki ; Zsuzsa Márka ; Szabolcs Márka ; Andrew B. MunkacsiSource :
- Journal of lipid research [ 1539-7262 ] ; 2020.
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
Links to Exploration step
pubmed:32457038Le document en format XML
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<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>
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<term>Receptors, Virus</term>
<term>Spike Glycoprotein, Coronavirus</term>
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<term>Intracellular Signaling Peptides and Proteins</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Receptors, Virus</term>
<term>Spike Glycoprotein, Coronavirus</term>
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<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Betacoronavirus</term>
<term>Lysosomes</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronavirus Infections</term>
<term>Niemann-Pick Disease, Type C</term>
<term>Pneumonia, Viral</term>
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<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Coronavirus Infections</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>
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<Title>Journal of lipid research</Title>
<ISOAbbreviation>J Lipid Res</ISOAbbreviation>
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<ArticleTitle>Potential COVID-19 therapeutics from a rare disease: weaponizing lipid dysregulation to combat viral infectivity.</ArticleTitle>
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<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>
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<AffiliationInfo><Affiliation>School of Biological Sciences and Centre for Biodiscovery, Victoria University of Wellington, Wellington 6012, New Zealand.</Affiliation>
</AffiliationInfo>
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</AffiliationInfo>
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