Influenza virus recruits host protein kinase C to control assembly and activity of its replication machinery

• DOI: 10.7554/elife.26910
• Publication Date: 2017-07-31T12:00:11Z
• Authors: Arindam Mondal; Anthony R Dawson; Gregory K Potts; Elyse C Freiberger; Steven F Baker; Lindsey A Moser; Kristen A Bernard; Joshua J Coon; Andrew Mehle
• Keywords: Nucleoprotein; Transcription; Viral structural protein

Influenza virus expresses transcripts early in infection and transitions towards genome replication at later time points. This process requires de novo assembly of the viral machinery, large ribonucleoprotein complexes (RNPs) composed polymerase, genomic RNA oligomeric nucleoprotein (NP). Despite central role RNPs during infection, factors dictating where when they assemble are poorly understood. Here we demonstrate that human protein kinase C (PKC) family members regulate RNP assembly. Activated PKCδ interacts with polymerase subunit PB2 phospho-regulates NP oligomerization infection. Consistent its regulating assembly, knockout impairs by selectively disrupting replication. However, primary transcription from pre-formed deposited infecting particles is unaffected. Thus, influenza exploits host PKCs to a step required for transition infectious cycle.