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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
How hepatitis C virus invades hepatocytes: the mystery of viral entry
Yong-Zhe Zhu1, Xi-Jing Qian1, Ping Zhao1
1Yong-Zhe Zhu, Xi-Jing Qian, Ping Zhao, Zhong-Tian Qi, Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China.
Insights
Hepatitis C virus (HCV) entry into liver cells involves key receptors like CD81 and claudin-1, plus kinases regulating infection. This review details these mechanisms and potential antiviral targets.
Area of Science:
- Virology
- Cell Biology
- Hepatology
Background:
- Hepatitis C virus (HCV) infection affects 170 million globally.
- HCV cell entry is a complex, multi-step process crucial for infection.
- Hepatocytes are the primary target cells for HCV.
Purpose of the Study:
- To review the mechanisms of HCV cell entry.
- To summarize the role of cellular receptors and kinases in HCV infection.
- To introduce potential antiviral strategies targeting HCV entry.
Main Methods:
- Literature review of scientific publications on HCV entry.
- Analysis of cellular factors involved in viral attachment, internalization, and fusion.
- Examination of host cell kinase regulation of HCV entry.
Main Results:
- Key receptors mediating HCV entry include scavenger receptor class B type I, CD81, claudin-1, and occludin.
- Receptor tyrosine kinases like EGFR and Ephrin A2 act as entry regulators.
- Host cell kinases play a significant role in modulating HCV entry processes.
Conclusions:
- Understanding HCV entry mechanisms is vital for developing effective antiviral therapies.
- Targeting specific cell surface molecules and kinases offers promising therapeutic avenues.
- Further research into HCV-host interactions can lead to novel treatment strategies.
Abstract:
Hepatitis C virus (HCV) infection is a global health problem, with an estimated 170 million people being chronically infected. HCV cell entry is a complex multi-step process, involving several cellular factors that trigger virus uptake into the hepatocytes. The high- density lipoprotein receptor scavenger receptor class B type I, tetraspanin CD81, tight junction protein claudin-1, and occludin are the main receptors that mediate the initial step of HCV infection. In addition, the virus uses cell receptor tyrosine kinases as entry regulators, such as epidermal growth factor receptor and ephrin receptor A2. This review summarizes the current understanding about how cell surface molecules are involved in HCV attachment, internalization, and membrane fusion, and how host cell kinases regulate virus entry. The advances of the potential antiviral agents targeting this process are introduced.
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