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. Author manuscript; available in PMC: 2015 Jan 10.
Published in final edited form as: J Pharmacogenomics Pharmacoproteomics. 2014 Sep 30;5(4):1000141. doi: 10.4172/2153-0645.1000141

Table 1.

Free radicals generated in response to respiratory viral infections.

Virus Free radical generated Effect Host proteins associated with oxidative stress Ref
Rhinovirus superoxide (O2−), hydrogen peroxide (H2O2) airway inflammation activation of xanthine oxidase; reduced concentration of glutathione (GSH) and increased activity of NADPH oxidase 1 (NOX1) [59,84–87]
Influenza Virus O2−, nitric oxide (NO) enhanced viral mutations, replication and airway inflammation reduced concentrations of catalase, glutathione and super oxide dismutase (SOD); Increased activity of NADPH oxidase 2 (NOX2) [60,66,88–91]
RSV NO, O2−, H2O2 airway inflammation virus induced nitric oxide synthase (iNOS) activity; progressive decrease of antioxidant enzymes SOD 1, SOD 3 and Catalase; reduced nuclear translocation of Nrf2 and Nrf2-ARE driven transcription [8,11,52,92] (Casola A, unpublished observation)
hMPV O2−, H2O2 airway inflammation progressive decrease of antioxidant enzymes SOD 3, catalase, GST, and Prdx; reduced nuclear translocation of Nrf2 and Nrf2-ARE driven transcription [11,63] (Casola A, unpublished observation)