Endocytosis of hepatitis C virus non-enveloped capsid-like particles induces MAPK–ERK1/2 signaling events
Identifieur interne : 001724 ( Main/Exploration ); précédent : 001723; suivant : 001725Endocytosis of hepatitis C virus non-enveloped capsid-like particles induces MAPK–ERK1/2 signaling events
Auteurs : Konstantina Katsarou [Grèce] ; Alexandros Lavdas [Grèce] ; Panagiota Tsitoura [Grèce] ; Elisavet Serti [Grèce] ; Panagiotis Markoulatos [Grèce] ; Penelope Mavromara [Grèce] ; Urania Georgopoulou [Grèce]Source :
- Cellular and Molecular Life Sciences [ 1420-682X ] ; 2010-07-01.
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Abstract
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.
Url:
DOI: 10.1007/s00018-010-0351-5
Affiliations:
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