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The hepatitis C virus (HCV) entry process is a complex, multi-step mechanism that enables the virus to infect hepatocytes. It involves sequential interactions with several host cell surface molecules, including glycosaminoglycans (GAGs), the low-density lipoprotein receptor (LDLR), scavenger receptor class B type I (SR-BI), tetraspanin CD81, claudin-1 (CLDN1), and occludin (OCLN). These interactions facilitate viral attachment, internalization via clathrin-mediated endocytosis, and fusion with endosomal membranes, leading to the release of the viral RNA genome into the cytoplasm. Because it involves multiple host molecules, it is a key antiviral target.
Inhibition of viral attachment, receptor binding, endocytosis, or fusion
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