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A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
Published on: May 10, 2022
Acquired apolipoprotein B deficiency with chronic hepatitis C virus infection
Insights
Hepatitis C virus (HCV) infection can cause fatty liver and acquired Apolipoprotein B (ApoB) deficiency. Treating HCV improved lipid profiles and ApoB levels in patients with this condition.
Area of Science:
- Hepatology
- Lipid Metabolism
- Virology
Background:
- Chronic hepatitis C virus (HCV) infection is frequently linked to hepatic steatosis (fatty liver).
- Apolipoprotein B (ApoB) deficiency is an established cause of fatty liver disease.
- Acquired ApoB deficiency has been recently associated with HCV infection.
Observation:
- Two patients presented with asymptomatic transaminase elevation, fatty liver, and high HCV viral load (genotype 3).
- Both patients exhibited abnormal lipid profiles, including low total cholesterol, low-density lipoprotein (LDL), triglycerides, and ApoB levels.
Findings:
- The study observed a correlation between HCV infection and acquired ApoB deficiency in the presented cases.
- Treatment of HCV infection in one patient led to improvements in their lipid profile and ApoB levels.
Implications:
- This case series suggests a potential link between HCV infection, particularly genotype 3, and acquired ApoB deficiency.
- Effective HCV treatment may reverse or improve lipid abnormalities and ApoB deficiency associated with the infection.
- Further research is warranted to elucidate the mechanisms underlying HCV-associated ApoB deficiency and its clinical significance.
Abstract:
Chronic hepatitis C virus (HCV) infection is often associated with fatty liver. Apolipoprotein B (ApoB) deficiency is one of the known causes of fatty liver and acquired ApoB deficiency has recently been reported with HCV infection. We report two patients (47-year-old lady and 48-year-old man) who had asymptomatic transaminase elevation, fatty liver, anti-HCV positive with high viral load (genotype 3). Their lipid profile showed low total cholesterol, low-density lipoprotein, triglycerides and ApoB. One of the patients who received treatment for HCV infection showed improvement in lipid profile and ApoB levels.
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