HCV infection is a major risk factor for liver cancer and liver transplantation worldwide. Overstimulation of host lipid metabolism in the liver by HCV-encoded proteins during viral infection creates a favorable environment for virus... more
HCV infection is a major risk factor for liver cancer and liver transplantation worldwide. Overstimulation of host lipid metabolism in the liver by HCV-encoded proteins during viral infection creates a favorable environment for virus propagation and pathogenesis. In this study, we hypothesize that targeting cellular enzymes acting as master regulators of lipid homeostasis could represent a powerful approach to developing
Research Interests: Microbiology, Immunology, Medical Microbiology, Membrane Proteins, Hepatitis C, and 21 moreHumans, Fatty acids, Cholesterol, Drug Design, Hepatitis C Virus, Liver Transplantation, Lipid metabolism, Risk factors, Enzyme, Fatty Liver, Spectrum, Specific Activity, Protease Inhibitors, Viral Infection, Fatty Acid, Risk Factors, Liver cancer, Metabolic pathway, Standard of Care, Antiviral Agents, and Proteolytic activity
Research Interests:
Research Interests: Hepatology, Humans, Female, Male, Young Adult, and 6 moreIncidence, British Columbia, Clinical Sciences, Aged, Middle Aged, and Adult
Research Interests:
Research Interests:
HCV infection is a major risk factor for liver cancer and liver transplantation worldwide. Overstimulation of host lipid metabolism in the liver by HCV-encoded proteins during viral infection creates a favorable environment for virus... more
HCV infection is a major risk factor for liver cancer and liver transplantation worldwide. Overstimulation of host lipid metabolism in the liver by HCV-encoded proteins during viral infection creates a favorable environment for virus propagation and pathogenesis. In this study, we hypothesize that targeting cellular enzymes acting as master regulators of lipid homeostasis could represent a powerful approach to developing a novel class of broad-spectrum antivirals against infection associated with human Flaviviridae viruses such as hepatitis C virus (HCV), whose assembly and pathogenesis depend on interaction with lipid droplets (LDs). One such master regulator of cholesterol metabolic pathways is the host subtilisin/kexin-isozyme-1 (SKI-1)--or site-1 protease (S1P). SKI-1/S1P plays a critical role in the proteolytic activation of sterol regulatory element binding proteins (SREBPs), which control expression of the key enzymes of cholesterol and fatty-acid biosynthesis. Here we report...