Hepatitis C Virus Entry Depends on Clathrin-Mediated Endocytosis

By Emmanuelle Blanchard, S. Belouzard, Lucie Goueslain, T. Wakita, J. Dubuisson, C. Wychowski, Y. Rouillé. Journal of Virology, 2006

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Screening of an FDA-Approved Compound Library Identifies Four Small-Molecule Inhibitors of Middle East Respiratory Syndrome Coronavirus Replication in Cell Culture (2014, background): “CPZ affects the assembly of clathrin-coated pits at the plasma membrane (56) and has been reported to inhibit the replication of alphaviruses (68), hepatitis C virus (69), and the coronaviruses SARS-CoV (70), infectious bronchitis virus (71), and MHV-2 (72).”
EGFR and EphA2 are host factors for hepatitis C virus entry and possible targets for antiviral therapy (2011, positive): “The observations that erlotinib inhibits late steps in the kinetic infection assay and in the HCV cell fusion assay suggest a functional role for EGFR in pH-dependent fusion of viral and host cell membrane”
SARS coronavirus entry into host cells through a novel clathrin- and caveolae-independent endocytic pathway (2008, background): “Pseudoviruses are often used to mimic the entry of real viruses, such as hepatitis C virus [18, 19] , Ebola virus, and Marburg virus [20] , into host cells.”