Hepatitis C virus (HCV) employs multiple strategies to subvert the host innate antiviral response
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Johannes G. Bode
Abstract
Hepatitis C virus (HCV) is a serious global health problem which accounts for approximately 40% of chronic liver diseases worldwide. HCV frequently establishes a persistent infection, although it is recognized and targeted by innate immunity as well as cellular and humoral immune mechanisms. This suggests that HCV has developed powerful strategies to escape elimination by innate and adaptive immunity. HCV-induced liver injury is thought to be mainly immune-mediated rather than due to direct cytopathic effects of the virus. Hence, therapeutic strategies should target those mechanisms favoring viral persistence since unspecific enhancement of host antiviral immunity may theoretically also promote liver injury. The present review summarizes our current understanding of how the hepatitis C virus interferes with the innate antiviral host-response to establish persistent infection.
©2008 by Walter de Gruyter Berlin New York
Artikel in diesem Heft
- Guest Editorial
- Highlight – Viruses and Signaling
- Highlight: Viruses and Signaling
- HIV-1 at the immunological and T-lymphocytic virological synapse
- Pursuing different ‘TRADDes’: TRADD signaling induced by TNF-receptor 1 and the Epstein-Barr virus oncoprotein LMP1
- RNA viruses and the mitogenic Raf/MEK/ERK signal transduction cascade
- Hepatitis C virus (HCV) employs multiple strategies to subvert the host innate antiviral response
- Sabotage of antiviral signaling and effectors by influenza viruses
- Influenza viruses and the NF-κB signaling pathway – towards a novel concept of antiviral therapy
- Genes and Nucleic Acids
- Specific inhibition of transcriptional activity of the constitutive androstane receptor (CAR) by the splicing factor SF3a3
- Generation of synthetic RNA-based thermosensors
- Molecular Medicine
- Impaired synthesis of heme oxygenase-1 in Fanconi anemia cells can be rescued by transfection of Fanconi wild-type cDNA
- Cell Biology and Signaling
- Effects of the Cdc2-like kinase-family and DNA topoisomerase I on the alternative splicing of eNOS in TNF-α-stimulated human endothelial cells
- Proteolysis
- Cytotoxic and peptidase inhibitory activities of selected non-hepatotoxic cyclic peptides from cyanobacteria
Artikel in diesem Heft
- Guest Editorial
- Highlight – Viruses and Signaling
- Highlight: Viruses and Signaling
- HIV-1 at the immunological and T-lymphocytic virological synapse
- Pursuing different ‘TRADDes’: TRADD signaling induced by TNF-receptor 1 and the Epstein-Barr virus oncoprotein LMP1
- RNA viruses and the mitogenic Raf/MEK/ERK signal transduction cascade
- Hepatitis C virus (HCV) employs multiple strategies to subvert the host innate antiviral response
- Sabotage of antiviral signaling and effectors by influenza viruses
- Influenza viruses and the NF-κB signaling pathway – towards a novel concept of antiviral therapy
- Genes and Nucleic Acids
- Specific inhibition of transcriptional activity of the constitutive androstane receptor (CAR) by the splicing factor SF3a3
- Generation of synthetic RNA-based thermosensors
- Molecular Medicine
- Impaired synthesis of heme oxygenase-1 in Fanconi anemia cells can be rescued by transfection of Fanconi wild-type cDNA
- Cell Biology and Signaling
- Effects of the Cdc2-like kinase-family and DNA topoisomerase I on the alternative splicing of eNOS in TNF-α-stimulated human endothelial cells
- Proteolysis
- Cytotoxic and peptidase inhibitory activities of selected non-hepatotoxic cyclic peptides from cyanobacteria
