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Updated: Jan 1, 2026
A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
Published on: May 10, 2022
Recent advances in hepatitis C virus cell entry
Birke Bartosch1,2,3, Jean Dubuisson4,5,6
1INSERM, U871, 69003 Lyon, France.
Insights
Hepatitis C virus (HCV) entry into liver cells involves complex interactions with host lipid metabolism. Understanding these molecular events and cellular co-factors is key to developing new antiviral strategies for chronic hepatitis C infection.
Area of Science:
- Virology
- Hepatology
- Molecular Biology
Background:
- Hepatitis C virus (HCV) chronically infects over 170 million people globally, leading to severe liver disease.
- Chronic HCV infection persists in 50-85% of patients, often resulting in fibrosis, cirrhosis, and hepatocellular carcinoma.
- HCV's unique life cycle and interaction with host lipid metabolism, particularly triglycerides, influence its presence with lipoproteins in patient serum.
Purpose of the Study:
- To review the molecular mechanisms of HCV cell entry.
- To elucidate the roles of cellular co-factors in HCV infection.
- To explore how lipoprotein association affects HCV entry.
Main Methods:
- Literature review focusing on molecular events in HCV cell entry.
- Analysis of the roles of identified cellular co-factors.
- Discussion of the impact of lipoprotein association on viral entry.
Main Results:
- HCV cell entry is a multi-step process involving specific cellular receptors.
- Key cellular co-factors implicated include low-density lipoprotein receptor, scavenger receptor BI, occludin, claudin-1, and CD81.
- HCV's association with lipoproteins appears to modulate its entry efficiency.
Conclusions:
- The interaction between HCV and host lipid metabolism is crucial for viral entry.
- Cellular co-factors play indispensable roles in mediating HCV attachment and entry.
- Further research into these interactions may reveal novel therapeutic targets for hepatitis C.
Abstract:
More than 170 million patients worldwide are chronically infected with hepatitis C virus (HCV). Prevalence rates range from 0.5% in Northern European countries to 28% in some areas of Egypt. HCV is hepatotropic, and in many countries chronic hepatitis C is a leading cause of liver disease including fibrosis, cirrhosis and hepatocellular carcinoma. HCV persists in 50-85% of infected patients, and once chronic infection is established, spontaneous clearance is rare. HCV is a member of the Flaviviridae family, in which it forms its own genus. Many lines of evidence suggest that the HCV life cycle displays many differences to that of other Flaviviridae family members. Some of these differences may be due to the close interaction of HCV with its host's lipid and particular triglyceride metabolism in the liver, which may explain why the virus can be found in association with lipoproteins in serum of infected patients. This review focuses on the molecular events underlying the HCV cell entry process and the respective roles of cellular co-factors that have been implied in these events. These include, among others, the lipoprotein receptors low density lipoprotein receptor and scavenger receptor BI, the tight junction factors occludin and claudin-1 as well as the tetraspanin CD81. We discuss the roles of these cellular factors in HCV cell entry and how association of HCV with lipoproteins may modulate the cell entry process.
