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The DR6 protein from human herpesvirus-6B induces p53-independent cell cycle arrest in G2/M

Mariane H Schleimann1, Søren Hoberg1, Aida Solhøj Hansen1

  • 1Department of Biomedicine, Aarhus University, Aarhus, Denmark.

Virology
|March 11, 2014
PubMed

Insights

Human herpesvirus 6B (HHV-6B) infection halts cell division. Researchers identified the direct repeat 6 (DR6) protein as a key inhibitor of G2/M cell-cycle progression, potentially explaining HHV-6B

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Human herpesvirus 6B (HHV-6B) infection is known to inhibit host cell proliferation.
  • The specific viral protein responsible for this G2/M cell-cycle arrest has not been identified.

Purpose of the Study:

  • To identify the HHV-6B protein that inhibits G2/M cell-cycle progression.
  • To elucidate the mechanism by which this protein affects cell division.

Main Methods:

  • Transfection and lentiviral transduction of the DR6 protein.
  • Analysis of cell proliferation, DNA synthesis, and cell-cycle distribution.
  • Western blotting and co-immunoprecipitation assays to study protein interactions.

Main Results:

  • The direct repeat 6 (DR6) protein was identified as an inhibitor of G2/M cell-cycle progression.
  • DR6 expression reduced cell numbers and inhibited DNA synthesis in a p53-independent and dose-dependent manner.
  • A specific N-terminal deletion in DR6 impaired nuclear translocation and DNA synthesis inhibition.
  • DR6 induced G2/M arrest with cytoplasmic accumulation of cyclin B1, which sequestered pCdk1.

Conclusions:

  • DR6 is a novel HHV-6B protein that inhibits host cell DNA synthesis and causes G2/M cell-cycle arrest.
  • DR6's mechanism involves regulating cyclin B1 and pCdk1 localization.
  • DR6 may play a significant role in the cytopathic effects of HHV-6B infection.
Keywords:
Direct repeat 6G2/M arrestHHV-6Human herpesvirus 6Bp53

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