1. Down-regulation of cellular protein heme oxygenase-1 inhibits proliferation of avian influenza virus H9N2 in chicken oviduct epithelial cells.
- Author
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Qi X, Zhang H, Xue T, Yang B, Deng M, and Wang J
- Subjects
- Adenoviridae genetics, Adenoviridae metabolism, Animals, Apoptosis drug effects, Avian Proteins agonists, Avian Proteins antagonists & inhibitors, Avian Proteins metabolism, Chickens, Epithelial Cells metabolism, Epithelial Cells virology, Female, Gene Expression Regulation, Genetic Vectors chemistry, Genetic Vectors metabolism, Heme Oxygenase-1 antagonists & inhibitors, Heme Oxygenase-1 metabolism, Host-Pathogen Interactions drug effects, Influenza A Virus, H9N2 Subtype, Mitochondria drug effects, Mitochondria metabolism, Oviducts metabolism, Oviducts virology, Oxidative Stress, Primary Cell Culture, RNA, Small Interfering genetics, RNA, Small Interfering metabolism, Reactive Oxygen Species agonists, Reactive Oxygen Species metabolism, Virus Replication drug effects, Avian Proteins genetics, Enzyme Inhibitors pharmacology, Epithelial Cells drug effects, Heme Oxygenase-1 genetics, Protoporphyrins pharmacology, Reactive Oxygen Species antagonists & inhibitors
- Abstract
The pathogenesis of H9N2 subtype avian influenza virus (AIV) infection in hens is often related to oviduct tissue damage. Our previous study suggested that H9N2 AIV induces cellular apoptosis by activating reactive oxygen species (ROS) accumulation and mitochondria-mediated apoptotic signalling in chicken oviduct epithelial cells (COECs). Heme oxygenase-1 (HO-1) is an inducible enzyme that exerts protective effects against oxidative stress and activated HO-1 was recently shown to have antiviral activity. To study the potential involvement of HO-1 in H9N2 AIV proliferation, the role of its expression in H9N2-infected COECs was further investigated. Our results revealed that H9N2 AIV infection significantly up-regulated the expression of HO-1 and that HO-1 down-regulation by ZnPP, a classical inhibitor of HO-1, could inhibit H9N2 AIV replication in COECs. Similarly, the small interfering RNA (siRNA)-mediated knockdown of HO-1 also markedly decreased the virus production in H9N2-infected COECs. In contrast, adenoviral-mediated over-expression of HO-1 concomitantly promoted H9N2 AIV replication. Taken together, our study demonstrated the involvement of HO-1 in AIV H9N2 proliferation, and these findings suggested that HO-1 is a potential target for inhibition of AIV H9N2 replication.
- Published
- 2018
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