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Potential Use of the Cholesterol Transfer Inhibitor U18666a As an Antiviral Drug for Research on Various Viral Infections Publisher Pubmed



Assefi M1 ; Bijan Rostami R2 ; Ebrahimi M3 ; Altafi M4 ; Tehrany PM5 ; Zaidan HK6 ; Talib Alnaqeeb BZ7 ; Hadi M8 ; Yasamineh S9 ; Gholizadeh O10
Authors
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Authors Affiliations
  1. 1. University of North Carolina at Greensboro, United States
  2. 2. School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Shahid Babai Faculty of Medicine, Qazvin University of Medical Sciences, Qazvin, Iran
  4. 4. Department of Microbiology, Faculty of Biological Science and Technology, Shiraz Pardis Branch, Islamic Azad University, Shiraz, Iran
  5. 5. Faculty of Medicine, National University of Malaysia, Bani, Malaysia
  6. 6. Department of Medical Laboratories Techniques, Al-Mustaqbal University College, Hillah, Babylon, Iraq
  7. 7. Anesthesia Technology Department, Al-Turath University College, Al Mansour, Baghdad, Iraq
  8. 8. Department of Basic Sciences, Tehran Central Branch, Islamic Azad University, Tehran, Iran
  9. 9. Department of Medical Biotechnology, Tabriz University of Medical Sciences, Tabriz, Iran
  10. 10. Department of Bacteriology and Virology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

Source: Microbial Pathogenesis Published:2023


Abstract

Cholesterol plays critical functions in arranging the biophysical attributes of proteins and lipids in the plasma membrane. For various viruses, an association with cholesterol for virus entrance and/or morphogenesis has been demonstrated. Therefore, the lipid metabolic pathways and the combination of membranes could be targeted to selectively suppress the virus replication steps as a basis for antiviral treatment. U18666A is a cationic amphiphilic drug (CAD) that affects intracellular transport and cholesterol production. A robust tool for investigating lysosomal cholesterol transfer and Ebola virus infection is an androstenolone derived termed U18666A that suppresses three enzymes in the cholesterol biosynthesis mechanism. In addition, U18666A inhibited low-density lipoprotein (LDL)-induced downregulation of LDL receptor and triggered lysosomal aggregation of cholesterol. According to reports, U18666A inhibits the reproduction of baculoviruses, filoviruses, hepatitis, coronaviruses, pseudorabies, HIV, influenza, and flaviviruses, as well as chikungunya and flaviviruses. U18666A-treated viral infections may act as a novel in vitro model system to elucidate the cholesterol mechanism of several viral infections. In this article, we discuss the mechanism and function of U18666A as a potent tool for studying cholesterol mechanisms in various viral infections. © 2023 Elsevier Ltd
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