Implications of oxidative stress on viral pathogenesis

Abstract

Reactive species are frequently formed after viral infections. Antioxidant defences, including enzymatic and non-enzymatic components, protect against reactive species, but sometimes these defences are not completely adequate. An imbalance in the production of reactive species and the body's inability to detoxify these reactive species is referred to as oxidative stress. The aim of this review is to analyse the role of oxidative stress in the pathogenesis of viral infections and highlight some major therapeutic approaches that have gained importance, with regards to controlling virus-induced oxidative injury. Attention will be focused on DNA viruses (papillomaviruses, hepadnaviruses), RNA viruses (flaviviruses, orthomyxoviruses, paramyxoviruses, togaviruses) and retroviruses (human immunodeficiency virus). In general, viruses cause an imbalance in the cellular redox environment, which depending on the virus and the cell can result in different responses, e.g. cell signaling, antioxidant defences, reactive species, and other processes. Therefore, the modulation of reactive species production and oxidative stress potentially represents a novel pharmacological approach for reducing the consequences of viral pathogenesis.

Protective Activity of Ascorbic Acid at Influenza Infection

“…Similarly, oxidative stress contri butes to the reproduction of human papillomavirus at several stages [62]. Data on the hepatitis C virus, however, are contradictory: there is evidence of both the inhibitory effect of oxidative stress on viral reproduction and the inhibitory pro perties of antioxidants [11].…”

“…They play an important role in the transfer of intercellular signal transduction, the regulation of cytokine production, growth and transcription factors, immunomodulation and apoptosis processes, etc. [11].…”

Coenzyme Q10 in acute influenza

“…The authors of the pediatric study also looked at total antioxidant capacity and found that it was decreased in both pandemic and seasonal influenza compared to controls. While we did not specifically evaluate total antioxidant capacity in our investigation, we do know that influenza infection causes excessive accumulation of reactive oxygen species which promote the inflammatory response via signaling pathways, ultimately leading to cell injury and contributing to overall influenza‐induced pathogenesis . Beyond this, Hennet et al .…”

Recent Advances in the Development of Antiviral Therapeutics for Rift Valley Fever Virus Infection

“…Cells and organisms must protect themselves against the deleterious effects of oxidation by reactive species generated both by insult and by normal cellular processes. Oxidative stress as a result of viral infection has been shown to be a contributor to pathogenesis [149]. Indeed, Narayanan et al demonstrated that the antioxidant enzyme superoxide dismutase 1 is downregulated at early time points after infection with RVFV, resulting in an increase of reactive oxygen species, as well as apoptosis in those cells [150].…”