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• W4254455428 abstract "Background and aim: Hepatitis C virus (HCV) is a major cause of chronic hepatitis worldwide. Toll-like receptors (TLRs) are pathogen recognition molecules that activate the innate immune system. Recognition of pathogen-associated molecular patterns (PAMPs) by TLRs induces the activation of genes important for an effective host defence. Previous studies show that TLRs are involved in the human host defence against viruses such as HSV, CMV, RSV and measles virus. In this study we aimed to elucidate whether TLR2 and 4 interact with HCV structural proteins. Methods: TLR2 and 4 activation was assessed in stably transfected HEK- and CHO cell lines following the incubation with recombinant HCV structural proteins. HCV-like particles (HCV-LPs)–generated by self-assembly of the HCV structural proteins in insect cells–were used as a well characterized model ligand for the study of virion-induced TLR2/4 interaction. Results: Our results show that recombinant C-terminally truncated core protein activates TLR2 transfected cells in a dose-dependent manner. By contrast, HCV-LPs or recombinant envelope proteins E1 and E2 did not result in transcriptional activation of TLR2 and TLR4 transfected CHO cells. Conclusion: Our findings suggest that monomeric core protein, but not core as part of the viral nucleocapsid or virion induces TLR2 signaling. It is conceivable that viral disassembly with degradation of nucleocapsids at distinct sites of the infected host may result in local HCV core-mediated TLR2 activation. Alternatively, unassembled core protein released from disintegrated infected hepatocytes may mediate the observed core-TLR2 interaction in vivo." @default.
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• W4254455428 date "2005-05-01" @default.
• W4254455428 modified "2023-09-25" @default.
• W4254455428 title "Hepatitis C Virus Structural Proteins and Activation of Toll-like Receptor 2 and 4" @default.
• W4254455428 doi "https://doi.org/10.1055/s-2005-920051" @default.
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