Working Paper Review Version 1 This version is not peer-reviewed

Reactive Oxygen Species (ROS) Homeostasis in Influenza Virus Infection

Version 1 : Received: 26 November 2019 / Approved: 27 November 2019 / Online: 27 November 2019 (04:20:30 CET)

How to cite: Chen, K.; Minakuchi, M.; Wuputra, K.; Ku, C.; Pan, J.; Kuo, K.; Lin, Y.; Saito, S.; Lin, C.; Yokoyama, K.K. Reactive Oxygen Species (ROS) Homeostasis in Influenza Virus Infection. Preprints 2019, 2019110328 Chen, K.; Minakuchi, M.; Wuputra, K.; Ku, C.; Pan, J.; Kuo, K.; Lin, Y.; Saito, S.; Lin, C.; Yokoyama, K.K. Reactive Oxygen Species (ROS) Homeostasis in Influenza Virus Infection. Preprints 2019, 2019110328

Abstract

Cellular oxidation is responsive to external and internal stimulation and is generated via signal molecules in defense mechanisms through networks of cell proliferation, differentiation, intracellular detoxification, bacterial infection, and immune reactions. Oxidative stress is not necessarily harmful per se; it depends on the balance between oxidation and antioxidation cascades, which are induced according to stimuli and can maintain oxygen homeostasis. The reactive oxygen species (ROS) that are generated during influenza virus (IV) infection have critical effects on both the virus and host cells. In this review, we outline the link between viral infection and ROS production, using IV as an example. We introduce the current state of knowledge on the molecular relationship between cellular oxidation mediated by ROS production and various effects of IV infection. We also summarize the potential anti-IV agents that act by targeting oxidative stress.

Subject Areas

antioxidation; aryl hydrocarbon receptor; cellular oxidation; nuclear factor E2-related factor 2; reactive oxygen species

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