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10.1194/jlr.R120000851

http://scihub22266oqcxt.onion/10.1194/jlr.R120000851
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32457038!7328045!32457038
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suck abstract from ncbi


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pmid32457038      J+Lipid+Res 2020 ; 61 (7): 972-982
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  • Potential COVID-19 therapeutics from a rare disease: weaponizing lipid dysregulation to combat viral infectivity #MMPMID32457038
  • Sturley SL; Rajakumar T; Hammond N; Higaki K; Marka Z; Marka S; Munkacsi AB
  • J Lipid Res 2020[Jul]; 61 (7): 972-982 PMID32457038show ga
  • 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.
  • |*Pandemics[MESH]
  • |Androstenes/therapeutic use[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Anticholesteremic Agents/*therapeutic use[MESH]
  • |Antiviral Agents/*therapeutic use[MESH]
  • |Betacoronavirus/*drug effects/metabolism/pathogenicity[MESH]
  • |COVID-19[MESH]
  • |Cholesterol/metabolism[MESH]
  • |Coronavirus Infections/diagnosis/*drug therapy/epidemiology[MESH]
  • |Drug Repositioning/methods[MESH]
  • |Humans[MESH]
  • |Hydroxychloroquine/therapeutic use[MESH]
  • |Intracellular Signaling Peptides and Proteins/antagonists & inhibitors/*genetics/metabolism[MESH]
  • |Lysosomes/drug effects/metabolism/virology[MESH]
  • |Niemann-Pick C1 Protein[MESH]
  • |Niemann-Pick Disease, Type C/*drug therapy/genetics/metabolism/pathology[MESH]
  • |Peptidyl-Dipeptidase A/genetics/metabolism[MESH]
  • |Pneumonia, Viral/diagnosis/*drug therapy/epidemiology[MESH]
  • |Protein Binding[MESH]
  • |Receptors, Virus/antagonists & inhibitors/genetics/metabolism[MESH]
  • |SARS-CoV-2[MESH]


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