c-Jun N-terminal kinase activity is required for efficient respiratory syncytial virus production

Leon Caly, Hong-Mei Li, Marie A. Bogoyevitch, David A. Jans

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4 Citations (Scopus)


Respiratory syncytial virus (RSV) is a major cause of respiratory infections in infants and the elderly, leading to more deaths than influenza each year worldwide. With no RSV antiviral or efficacious vaccine currently available, improved understanding of the host-RSV interaction is urgently required. Here we examine the contribution to RSV infection of the host stress-regulated c-Jun N-terminal kinase (JNK), for the first time. Peak JNK1/2 phosphoactivation is observed at ∼24 h post-infection, correlating with the time of virus assembly. The release of infectious RSV virions from infected cells was significantly reduced by either JNK1/2 siRNA knockdown or treatment with the JNK-specific inhibitor, JNK-IN-VIII. High resolution microscopy confirmed RSV accumulation in the host cell cytoplasm. The results implicate JNK1/2 as a key host factor for RSV virus production, raising the possibility of agents targeting JNK activity as potential anti-RSV therapeutics.

Original languageEnglish
Pages (from-to)64-68
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - 29 Jan 2017


  • c-Jun N-terminal kinase
  • JNK
  • Respiratory syncytial virus
  • Viral release

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