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Regulation of Mumps Virus Replication and Transcription by Kinase RPS6KB1

Kelsey Briggs1, Leyi Wang1, Kaito Nagashima1

  • 1Department of Infectious Diseases, University of Georgia College of Veterinary Medicine, Athens, Georgia, USA.

Journal of Virology
|April 17, 2020
PubMed

Insights

Mumps virus (MuV) reemerged in the US. Researchers found the human kinase ribosomal protein S6 kinase beta-1 (RPS6KB1) negatively regulates MuV replication and transcription, potentially via interaction with the MuV P protein.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Mumps virus (MuV), a Paramyxoviridae family member, causes viral meningitis and has recently reemerged in the US.
  • MuV replication relies on its RNA-dependent RNA polymerase (vRdRp), comprising the L and P proteins, and nucleocapsid protein (NP).
  • Host kinases phosphorylate the MuV P protein, influencing its function in viral replication and transcription.

Purpose of the Study:

  • To identify host kinases regulating MuV replication and transcription.
  • To elucidate the role of identified kinases in the MuV life cycle.
  • To explore potential therapeutic targets for mumps virus infections.

Main Methods:

  • A large-scale small interfering RNA (siRNA) screen targeting host kinases involved in MuV replication.
  • Validation of identified kinases using siRNA knockdown, specific inhibitors, and knockout cell lines.
  • Co-immunoprecipitation assays to detect protein-protein interactions between MuV proteins and host kinases.

Main Results:

  • The human kinase ribosomal protein S6 kinase beta-1 (RPS6KB1) was identified as a key regulator of MuV replication and transcription.
  • RPS6KB1 was found to negatively regulate MuV growth, with increased viral replication observed in RPS6KB1-deficient cells.
  • An interaction between the MuV P protein and RPS6KB1 was detected, suggesting a direct regulatory mechanism.

Conclusions:

  • RPS6KB1 negatively impacts Mumps virus replication and transcription, likely through direct interaction with the viral P protein.
  • This study reveals a novel mumps virus-host interaction, highlighting RPS6KB1 as a potential target for antiviral strategies.
  • Understanding this interaction could inform the development of new antiviral therapies and improve vaccine efficacy against reemerging mumps virus.
Keywords:
RPS6KB1kinasemumps virusreplication

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