Endocytosis of hepatitis C virus non-enveloped capsid-like particles induces MAPK–ERK1/2 signaling events |
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Authors: | Konstantina Katsarou Alexandros Α Lavdas Panagiota Tsitoura Elisavet Serti Panagiotis Markoulatos Penelope Mavromara Urania Georgopoulou |
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Institution: | (1) Molecular Virology Laboratory, Hellenic Pasteur Institute, Athens, Greece;(2) Laboratory of Cellular and Molecular Neurobiology, Hellenic Pasteur Institute, Athens, Greece;(3) Present address: Insect Molecular Genetics and Biotechnology, Institute of Biology, NCSR Demokritos, Athens, Greece;(4) Department of Biochemistry and Biotechnology, University of Thessaly, Thessaly, Greece; |
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Abstract: | Although HCV is an enveloped virus, naked nucleocapsids have been reported in the serum of infected patients. The HCV core
particle serves as a protective capsid shell for the viral genome and recombinant in vitro assembled HCV core particles induce
strong specific immunity. We investigated the post-binding mechanism of recombinant core particle uptake and its intracellular
fate. In hepatic cells, these particles are internalized, most likely in a clathrin-dependent pathway, reaching early to late
endosomes and finally lysosomes. The endocytic acidic milieu is implicated in trafficking process. Using specific phosphoantibodies,
signaling pathway inhibitors and chemical agents, ERK1/2 was found to be activated in a sustained way after endocytosis, followed by downstream immediate early genes (c-fos and egr-1) modulation. We propose that the intriguing properties of cellular internalization of HCV non-enveloped particles can induce
specific ERK1/2–MAPKs events that could be important in HCV life cycle and pathogenesis of HCV infection. |
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