Role of c-Jun terminal kinase (JNK) activation in influenza A virus-induced autophagy and replication

Jingting Zhang, Tao Ruan, Tianyu Sheng, Jiongjiong Wang, Jing Sun, Jin Wang, Richard A. Prinz, Daxin Peng, Xiufan Liu, Xiulong Xu

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


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. SP600125, 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.

Original languageEnglish (US)
Pages (from-to)1-12
Number of pages12
StatePublished - Jan 2 2019


  • Autophagy
  • Influenza A virus
  • JNK
  • NS1
  • PI-3 kinase

ASJC Scopus subject areas

  • Virology


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