Influenza A virus PB1-F2 is involved in regulation of cellular redox state in alveolar epithelial cells

Biochemical and Biophysical Research Communications
Nary ShinSang-Yun Choi

Abstract

Occurrence of oxidative stress is common in influenza, and renders the host more susceptible to pathogenic effects including cell death. We previously reported that down-regulation of superoxide anion dismutase 1 (SOD1) by influenza A virus (IAV) resulted in a significant increase in the levels of reactive oxygen species (ROS) and viral PB1 polymerase gene product in the early stage of infection. However, the precise molecular mechanism of IAV-mediated ROS generation is not yet fully understood. In this study, we investigated the possible involvement of the key virulence factor PB1-F2 in ROS generation and its contribution to the viral propagation and cell death. The key virulence factor PB1-F2 was found to be responsible, at least in part, for the ROS generation through lowering the SOD1 level in alveolar epithelial A549 cells. PB1-F2 overexpression resulted in SOD1 diminishment and ROS enhancement, while another virulent factor, NS1, did not show significant changes. Inversely, we examined the effects of the absence of PB1-F2 using mutant IAV lacking PB1-F2 expression (mutantΔF2). Infection with mutantΔF2 virus did not significantly lower the SOD1 level, and thus generated moderately low levels of ROS. In addition, the oxidat...Continue Reading

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Citations

Sep 24, 2016·Journal of Immunological Methods·Dejan KatanicJuilee Thakar
Mar 13, 2020·Cellular & Molecular Biology Letters·Mohsen KeshavarzFarhad Rezaei
Jul 22, 2020·BMC Microbiology·Ker-Kong ChenKazunari K Yokoyama
Jul 28, 2018·Viruses·Olga A KhomichAlexander V Ivanov
Nov 19, 2020·Vaccines·Irina V KiselevaLudmila V Puchkova
Jul 15, 2020·Cold Spring Harbor Perspectives in Medicine·Raquel Muñoz-MorenoAdolfo García-Sastre

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