Implication of nitric oxide in the pathogenesis of influenza virus infection

Abstract

Influenza continues to be a significant threat to global public health. Even annual vaccination fails to prevent complicated illness and death. The findings in various studies suggest that severe disease is attributed to pulmonary complications-primary viral and secondary bacterial pneumonia. A number of investigations on influenza virus infection in the mouse model demonstrate that overproduction of free radicals, including nitric oxide (NO), contributes to the development of pneumonia during influenza virus infection. The role of NO on influenza virus infection in mice and differences between inducible nitric oxide synthase activation in mouse and human systems are discussed in this review. The biosynthesis of NO, mechanisms for regulation of NO production, nitrative stress during pathogenesis of various microbial infections are overviewed as well.

Impact of Protein Nitration on Influenza Virus Infectivity and Immunogenicity

“…This nitrative stress has been linked directly to the pathogenesis of influenza disease in mice. iNOS knockout mice have increased survival following infection with influenza virus compared to iNOS-competent mice ( 17 , 20 ). This has also been observed with other pathogens, such as Sendai virus, Dengue virus, and Cryptococcus gattii ( 1 , 21 – 24 ).…”

In Vitro Evaluation of Anti-Rift Valley Fever Virus, Antioxidant and Anti-Inflammatory Activity of South African Medicinal Plant Extracts

“…High levels of ROS have been shown to activate nitric oxide synthase 2 (iNOS 2) for RNS production. The presence of nitric oxide (NO) is beneficial in that it has antiviral properties, but in surplus, it can promote the pathogenesis of herpes simplex virus 1 (HSV-1) [ 19 ], human immunodeficiency virus (HIV) [ 20 ], influenza virus [ 21 ] and RVFV [ 22 ] by damaging cells in host tissues. Oxidatively, NO reacts with superoxide anion to form a highly reactive anion called peroxynitrite (ONOO − ), which induces lipid peroxidation and nitro-tyrosination that disrupts the functioning of cells [ 14 ].…”