desmosterol/hepatitis

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Hepatitis C Virus Selectively Alters the Intracellular Localization of Desmosterol.

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Hepatitis C virus (HCV) increases intracellular desmosterol without affecting the steady-state abundance of other sterols, and the antiviral activity of inhibitors of desmosterol synthesis is suppressed by the addition of exogenous desmosterol. These observations suggest a model in which desmosterol

Desmosterol Increases Lipid Bilayer Fluidity during Hepatitis C Virus Infection.

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Hepatitis C virus (HCV) uniquely affects desmosterol homeostasis by increasing its intracellular abundance and affecting its localization. These effects are important for productive viral replication because the inhibition of desmosterol synthesis has an antiviral effect that can be rescued by the

Lipid metabolite profiling identifies desmosterol metabolism as a new antiviral target for hepatitis C virus.

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Hepatitis C virus (HCV) infection has been clinically associated with serum lipid abnormalities, yet our understanding of the effects of HCV on host lipid metabolism and conversely the function of individual lipids in HCV replication remains incomplete. Using liquid chromatography-mass spectrometry

Noncholesterol Sterols as Surrogate Markers in Patients with Severe Alcoholic Hepatitis.

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Severe alcoholic hepatitis (AH) is a life-threatening condition lacking good serologic markers to tailor treatment and predict recovery. We examined the cholesterol metabolism in severe AH to explore prognostic markers and evaluate the profile of cholesterol precursors, cholestanol and phytosterols,

Protective role of plant sterol and stanol esters in liver inflammation: insights from mice and humans.

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The inflammatory component of non-alcoholic steatohepatitis (NASH) can lead to irreversible liver damage. Therefore there is an urgent need to identify novel interventions to combat hepatic inflammation. In mice, omitting cholesterol from the diet reduced hepatic inflammation. Considering the

Hepatitis C virus NS3-4A protease regulates the lipid environment for RNA replication by cleaving host enzyme 24-dehydrocholesterol reductase

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Many RNA viruses create specialized membranes for genome replication by manipulating host lipid metabolism and trafficking, but in most cases, we do not know the molecular mechanisms responsible or how specific lipids may impact the associated membrane and viral process. For example, hepatitis C

Desmosterol and DHCR24: unexpected new directions for a terminal step in cholesterol synthesis.

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3β-Hydroxysterol Δ(24)-reductase (DHCR24) catalyzes the conversion of desmosterol to cholesterol. This ultimate step of cholesterol biosynthesis appears to be remarkable in its diverse functions and the number of diseases it is implicated in from vascular disease to Hepatitis C virus (HCV) infection

Prominent steatosis with hypermetabolism of the cell line permissive for years of infection with hepatitis C virus.

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Most of experiments for HCV infection have been done using lytic infection systems, in which HCV-infected cells inevitably die. Here, to elucidate metabolic alteration in HCV-infected cells in a more stable condition, we established an HCV-persistently-infected cell line, designated as HPI cells.

New chemotype of selective and potent inhibitors of human delta 24-dehydrocholesterol reductase.

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The enzyme Δ24-dehydrocholesterol reductase (DHCR24) catalyzes the reduction of the Δ24-double bond in the side chain of cholesterol precursors. Recent biochemical investigations fuel the hope that inhibition of DHCR24, resulting in an accumulation of desmosterol, can open new therapeutic options

Cholesterol precursors: more than mere markers of biosynthesis.

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OBJECTIVE Circulating levels of cholesterol precursors in the body have proven their value over the years as indicators of in-vivo cholesterol synthesis. However, there is growing interest in their potential as markers of various disease states. The purpose of this review is to evaluate current

Dysregulation of distal cholesterol biosynthesis in association with relapse and advanced disease in CHC genotype 2 and 3 treated with sofosbuvir and ribavirin.

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OBJECTIVE Hepatitis C virus (HCV) modulates host lipid metabolism for its replication and lifecycle. Our aims were to assess changes in the serum lipid and distal (post-squalene) cholesterol biosynthesis metabolite profile of HCV genotypes (GT) 2 and 3 patients treated with

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