Abstract
Reactive oxygen species (ROS) are well known for being both beneficial and deleterious. The main thrust of this review is to investigate the role of ROS in ribonucleic acid (RNA) virus pathogenesis. Much evidences has accumulated over the past decade, suggesting that patients infected with RNA viruses are under chronic oxidative stress. Changes to the body's antioxidant defense system, in relation to SOD, ascorbic acid, selenium, carotenoids, and glutathione, have been reported in various tissues of RNA-virus infected patients. This review focuses on RNA viruses and retroviruses, giving particular attention to the human influenza virus, Hepatitis c virus (HCV), human immunodeficiency virus (HIV), and the aquatic Betanodavirus. Oxidative stress via RNA virus infections can contribute to several aspects of viral disease pathogenesis including apoptosis, loss of immune function, viral replication, inflammatory response, and loss of body weight. We focus on how ROS production is correlated with host cell death. Moreover, ROS may play an important role as a signal molecule in the regulation of viral replication and organelle function, potentially providing new insights in the prevention and treatment of RNA viruses and retrovirus infections.
Highlights
Cellular metabolisms produce different varieties of reactive oxygen species (ROS) as byproducts
This supports previous research related to the involvement of oxidative stress in cell deaths caused during ribonucleic acid (RNA) virus infection
Current studies of ROS are based on the lethal effects of ROS in various diseases such as cancer, human immunodeficiency virus (HIV), hepatitis, and diabetes
Summary
Cellular metabolisms produce different varieties of reactive oxygen species (ROS) as byproducts. The research has shown that children suffering from hepatitis B or C exhibit increased levels of lipid peroxidation, which indicates weak antioxidant defense due to low catalase and SOD activity [9]. Earlier and recent studies have suggested that ROS induces apoptosis [10,11,12], and that the agents that cause apoptosis are either oxidants or generate the ROS This hypothesis was later shown to be correct when researchers demonstrated the role of proto-oncogene BCL-2 in preventing apoptosis in an antioxidant way [13]. The pro-antioxidant effect of TNF may be relevant to influenza virus infection because children with Rey’s syndrome [40] exhibit increased levels of pro-oxidants and lipid peroxides. Immune system cells generally require a higher concentration of antioxidants than other cells to maintain the system’s rodex balance and preserve its integrity and function
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