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Elife. 2017 Jul 31;6. pii: e26910. doi: 10.7554/eLife.26910. [Epub ahead of print]
Influenza virus recruits host protein kinase C to control assembly and activity of its replication machinery.
Mondal A1, Dawson AR2, Potts GK3, Freiberger EC4, Baker SF2, Moser LA5, Bernard KA5, Coon JJ3, Mehle A2.
Author information
Abstract
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 replication machinery, large ribonucleoprotein complexes (RNPs) composed of the viral polymerase, genomic RNA and oligomeric nucleoprotein (NP). Despite the central role of RNPs during infection, the factors dictating where and when they assemble are poorly understood. Here we demonstrate that human protein kinase C (PKC) family members regulate RNP assembly. Activated PKCδ interacts with the polymerase subunit PB2 and phospho-regulates NP oligomerization and RNP assembly during infection. Consistent with its role in regulating RNP assembly, knockout of PKCδ impairs virus infection by selectively disrupting genome replication. However, primary transcription from pre-formed RNPs deposited by infecting particles is unaffected. Thus, influenza virus exploits host PKCs to regulate RNP assembly, a step required for the transition from primary transcription to genome replication during the infectious cycle.
KEYWORDS:
human; infectious disease; microbiology
PMID: 28758638 DOI: 10.7554/eLife.26910
Influenza virus recruits host protein kinase C to control assembly and activity of its replication machinery.
Mondal A1, Dawson AR2, Potts GK3, Freiberger EC4, Baker SF2, Moser LA5, Bernard KA5, Coon JJ3, Mehle A2.
Author information
Abstract
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 replication machinery, large ribonucleoprotein complexes (RNPs) composed of the viral polymerase, genomic RNA and oligomeric nucleoprotein (NP). Despite the central role of RNPs during infection, the factors dictating where and when they assemble are poorly understood. Here we demonstrate that human protein kinase C (PKC) family members regulate RNP assembly. Activated PKCδ interacts with the polymerase subunit PB2 and phospho-regulates NP oligomerization and RNP assembly during infection. Consistent with its role in regulating RNP assembly, knockout of PKCδ impairs virus infection by selectively disrupting genome replication. However, primary transcription from pre-formed RNPs deposited by infecting particles is unaffected. Thus, influenza virus exploits host PKCs to regulate RNP assembly, a step required for the transition from primary transcription to genome replication during the infectious cycle.
KEYWORDS:
human; infectious disease; microbiology
PMID: 28758638 DOI: 10.7554/eLife.26910