The cellular stress response in hepatitis C virus infection: A balancing act to promote viral persistence and host cell survival.
Virus Res
; 263: 1-8, 2019 04 02.
Article
in En
| MEDLINE
| ID: mdl-30599163
ABSTRACT
Oxidative- and endoplasmic reticulum (ER)-stress are common events during hepatitis C virus (HCV) infection and both regulate cell survival and determine clinical outcome. In response to intrinsic and extrinsic cellular stress, different adaptive mechanisms have evolved in hepatocytes to restore cellular homeostasis like the anti-oxidant response, the unfolded protein response (UPR) and the integrated stress response (ISR). In this review, we focus on the cellular stress response in the context of acute and chronic HCV infection. The mechanisms of induction and modulation of oxidative- and ER-stress are reviewed and analyzed from both perspectives viral persistence and cell survival. Besides, we delve into the activation of the eIF2α/ATF4 pathway and selective autophagy induction; pathways involved in the elimination of harmful viral proteins after oxidative stress induction. For this, the negative role of autophagy upon HCV infection or negative regulation of viral replication is analyzed. Finally, we hypothesize that the cellular stress response in hepatocytes plays a major role for HCV control thus acting as an important host-factor for virus clearance during the early stages of HCV infection.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Stress, Physiological
/
Hepatitis C
/
Oxidative Stress
/
Hepatocytes
/
Host-Pathogen Interactions
/
Endoplasmic Reticulum Stress
Limits:
Humans
Language:
En
Journal:
Virus Res
Journal subject:
VIROLOGIA
Year:
2019
Document type:
Article