NDLI: Look who’s talking—the crosstalk between oxidative stress and autophagy supports exosomal-dependent release of HCV particles

Content Provider	Springer Nature Link
Author	Medvedev, Regina Hildt, Eberhard Ploen, Daniela
Copyright Year	2016
Abstract	Autophagy is a highly conserved and regulated intracellular lysosomal degradation pathway that is essential for cell survival. Dysregulation has been linked to the development of various human diseases, including neurodegeneration and tumorigenesis, infection, and aging. Besides, many viruses hijack the autophagosomal pathway to support their life cycle. The hepatitis C virus (HCV), a major cause of chronic liver diseases worldwide, has been described to induce autophagy. The autophagosomal pathway can be further activated in response to elevated levels of reactive oxygen species (ROS). HCV impairs the Nrf2/ARE-dependent induction of ROS-detoxifying enzymes by a so far unprecedented mechanism. In line with this, this review aims to discuss the relevance of HCV-dependent elevated ROS levels for the induction of autophagy as a result of the impaired Nrf2 signaling and the described crosstalk between p62 and the Nrf2/Keap1 signaling pathway. Moreover, autophagy is functionally connected to the endocytic pathway as components of the endosomal trafficking are involved in the maturation of autophagosomes. The release of HCV particles is still not fully understood. Recent studies suggest an involvement of exosomes that originate from the endosomal pathway in viral release. In line with this, it is tempting to speculate whether HCV-dependent elevated ROS levels induce autophagy to support exosome-mediated release of viral particles. Based on recent findings, in this review, we will further highlight the impact of HCV-induced autophagy and its interplay with the endosomal pathway as a novel mechanism for the release of HCV particles.
Starting Page	211
Ending Page	231
Page Count	21
File Format	PDF
ISSN	07422091
Journal	Cell Biology and Toxicology
Volume Number	33
Issue Number	3
e-ISSN	15736822
Language	English
Publisher	Springer Netherlands
Publisher Date	2016-12-16
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Autophagy Endosomal/exosomal trafficking Hepatitis C virus Nrf2/Keap1-signaling p62 Reactive oxygen species (ROS) Cell Biology Pharmacology/Toxicology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Health, Toxicology and Mutagenesis Toxicology

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