期刊
VIROLOGY
卷 526, 期 -, 页码 1-12出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2018.09.020
关键词
Influenza A virus; Autophagy; NS1; JNK; PI-3 kinase
类别
资金
- College of Veterinary Medicine, Yangzhou University
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- China Postdoctoral Science Foundation [2015M581873]
- Natural Science Foundation of Jiangsu Province [BK20150450]
- Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry [2015311]
The non-structural protein 1 (NS1) of different influenza A virus (IAV) strains can differentially regulate the activity of c-Jun terminal kinase (JNK) and PI-3 kinase (PI3K). Whether varying JNK and PI3K activation impacts autophagy and IAV replication differently remains uncertain. Here we report that H5N1 (A/mallard/Huadong/S/2005) influenza A virus induced functional autophagy, as evidenced by increased LC3 lipidation and decreased p62 levels, and the presence of autolysosomes in chicken fibroblast cells. H9N2 (A/chicken/Shanghai/F/98) virus weakly induced autophagy, whereas H1N1 virus (A/PR/8/34, PR8) blocked autophagic flux. H5N1 virus activated JNK but inhibited the PI-3 kinase pathway. In contrast, N9N2 virus infection led to modest JNK activation and strong PI-3 kinase activation; whereas H1N1 virus activated the PI-3 kinase pathway but did not activate JNK. 5P600125, a JNK inhibitor, inhibited H5N1 virus-induced autophagy and virus replication in a DF-1 chicken fibroblast cell line. Our study uncovered a previously unrecognized role of JNK in IAV replication and autophagy.
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