Flaviviridae Viruses and Oxidative Stress: Implications for Viral Pathogenesis

Abstract

Oxidative stress is induced once the balance of generation and neutralization of reactive oxygen species (ROS) is broken in the cell, and it plays crucial roles in a variety of natural and diseased processes. Infections of Flaviviridae viruses trigger oxidative stress, which affects both the cellular metabolism and the life cycle of the viruses. Oxidative stress associated with specific viral proteins, experimental culture systems, and patient infections, as well as its correlations with the viral pathogenesis attracts much research attention. In this review, we primarily focus on hepatitis C virus (HCV), dengue virus (DENV), Zika virus (ZIKV), Japanese encephalitis virus (JEV), West Nile virus (WNV), and tick-borne encephalitis virus (TBEV) as representatives of Flaviviridae viruses and we summarize the mechanisms involved in the relevance of oxidative stress for virus-associated pathogenesis. We discuss the current understanding of the pathogenic mechanisms of oxidative stress induced by Flaviviridae viruses and highlight the relevance of autophagy and DNA damage in the life cycle of viruses. Understanding the crosstalk between viral infection and oxidative stress-induced molecular events may offer new avenues for antiviral therapeutics.

Oxidative stress, immunological and cellular hypoxia biomarkers in hepatitis C treatment-naïve and cirrhotic patients

“…Biomarkers of oxidative stress are increased in liver tissue and body fluids of patients with chronic HCV infection. Induction of oxidative stress correlates with the incidence and/or severity of HCV-related morbidities, since chronic HCV infection relies on this strategy for immune escape and persistence [5][6][7][8]. In support, antioxidants were promising co-adjuvants in HCV therapy [27].…”

“…One pathogenic mechanism for HCV is oxidative stress resultant from increased generation of reactive oxygen species in infected hepatocytes, where redox homeostatic balance is a major challenge to prevent cell death and DNA mutation [4][5][6][7][8]. Mechanistically, HCV activates prooxidant enzymes and hepatic stellate cells, weakens antioxidant defenses, and induces organelle damage, secretion of pro-inflammatory cytokines and metals unbalance -secondary to mitochondrial failure, which is a focal point in that scenario [9,10].…”

Changes in Oxidation-antioxidation Function on the Thymus of Chickens Infected with Reticuloendotheliosis Virus

“…Under conditions of oxidative stress, ROS and RNS promote the accumulation of lipid peroxidation in polyunsaturated fatty acids in oxidized bio lms, and produce lipid peroxides (e.g., MDA, ketone, hydroxyl, and carboxyl) [22]. Moreover, MDA can re ect the degree of lipid peroxidation in the body and can be used as an indicator to determine whether a cell is oxidatively damaged [23].…”

Natural Antioxidants: A Review of Studies on Human and Animal Coronavirus

“…In order to counterbalance the oxidant species, there is an antioxidant system formed by enzymes and nonenzymatic molecules [ 19 , 20 ]. However, during pathological events, such as viral infections, there may be an increase in the production of oxidant species not neutralized by the antioxidant system, resulting in oxidative stress that promotes cellular damage through protein denaturation, changes in the functions of nucleic acids, lipid peroxidation, and cell death [ 21 – 23 ].…”