Counteraction of HCV-Induced Oxidative Stress Concurs to Establish Chronic Infection in Liver Cell Cultures
Joint Authors
Anticoli, Simona
Amatore, Donatella
Matarrese, Paola
De Angelis, Marta
Ruggieri, Anna
Nencioni, Lucia
Palamara, Anna Teresa
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-02-13
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract EN
Hepatitis C virus (HCV) is a blood-borne pathogen causing acute and chronic hepatitis.
A significant number of people chronically infected with HCV develop cirrhosis and/or liver cancer.
The pathophysiologic mechanisms of hepatocyte damage associated with chronic HCV infection are not fully understood yet, mainly due to the lack of an in vitro system able to recapitulate the stages of infection in vivo.
Several studies underline that HCV virus replication depends on redox-sensitive cellular pathways; in addition, it is known that virus itself induces alterations of the cellular redox state.
However, the exact interplay between HCV replication and oxidative stress has not been elucidated.
In particular, the role of reduced glutathione (GSH) in HCV replication and infection is still not clear.
We set up an in vitro system, based on low m.o.i.
of Huh7.5 cell line with a HCV infectious clone (J6/JFH1), that reproduced the acute and persistent phases of HCV infection up to 76 days of culture.
We demonstrated that the acute phase of HCV infection is characterized by the elevated levels of reactive oxygen species (ROS) associated in part with an increase of NADPH-oxidase transcripts and activity and a depletion of GSH accompanied by high rates of viral replication and apoptotic cell death.
Conversely, the chronic phase is characterized by a reestablishment of reduced environment due to a decreased ROS production and increased GSH content in infected cells that might concur to the establishment of viral persistence.
Treatment with the prooxidant auranofin of the persistently infected cultures induced the increase of viral RNA titer, suggesting that a prooxidant state could favor the reactivation of HCV viral replication that in turn caused cell damage and death.
Our results suggest that targeting the redox-sensitive host-cells pathways essential for viral replication and/or persistence may represent a promising option for contrasting HCV infection.
American Psychological Association (APA)
Anticoli, Simona& Amatore, Donatella& Matarrese, Paola& De Angelis, Marta& Palamara, Anna Teresa& Nencioni, Lucia…[et al.]. 2019. Counteraction of HCV-Induced Oxidative Stress Concurs to Establish Chronic Infection in Liver Cell Cultures. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1204628
Modern Language Association (MLA)
Anticoli, Simona…[et al.]. Counteraction of HCV-Induced Oxidative Stress Concurs to Establish Chronic Infection in Liver Cell Cultures. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-14.
https://search.emarefa.net/detail/BIM-1204628
American Medical Association (AMA)
Anticoli, Simona& Amatore, Donatella& Matarrese, Paola& De Angelis, Marta& Palamara, Anna Teresa& Nencioni, Lucia…[et al.]. Counteraction of HCV-Induced Oxidative Stress Concurs to Establish Chronic Infection in Liver Cell Cultures. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1204628
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1204628