RNA Viruses: ROS-Mediated Cell Death

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.

Figure 1

Schematic diagram of apoptotic cascade and the sites of action of general and specific caspases. The figure also illustrates how ROS produced during viral infection can affect apoptotic cascades. Abbreviations used in figure: FAS/TNF-α: tumor necrosis factor alpha (death receptors); FADD: Fas associated death domain; TRADD: tumor necrosis factor receptor associated death domain; Cas: caspase; AIF: apoptosis-inducing factor; PARP: poly (ADP) ribose polymerase; EndoG: endonuclease G; DFF-40: DNA fragmentation factor 40 KDa; tBID: truncated BID; DISC: death-inducing signaling complex.

Figure 2

Effects of reactive oxygen species on different areas.