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Roseoloviruses manipulate host cell cycle

Niza Frenkel1, Eyal Sharon1, Haim Zeigerman1

  • 1Department of Cell Research and Immunology and the S. Daniel Abraham Institute for Molecular Virology, Tel Aviv University, Tel Aviv 69978, Israel.

Current Opinion in Virology
|December 3, 2014
PubMed

Insights

Human herpesvirus 6 (HHV-6A/B) hijacks cell cycle regulation by degrading Rb, releasing E2F1 to promote viral DNA replication. Roseoloviruses induce cell cycle arrest, impacting viral replication strategies.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Human herpesvirus 6 (HHV-6A and HHV-6B) are ubiquitous viruses known to establish lifelong infections.
  • Lytic HHV-6 infections involve complex interactions with host cell machinery, including cell cycle regulation.
  • The E2F1 transcription factor and its regulatory partners play critical roles in cell cycle progression.

Purpose of the Study:

  • To investigate the role of E2F1 transcription factor in HHV-6A and HHV-6B lytic infections.
  • To identify HHV-6 genes regulated by E2F1.
  • To understand how HHV-6 manipulates host cell cycle for viral replication.

Main Methods:

  • Analysis of E2F1-Rb complex disruption during HHV-6 infection.
  • Quantitative assessment of E2F1 and DP1 expression post-infection.
  • Identification of E2F binding sites in HHV-6 gene promoters using techniques like ChIP-seq or promoter analysis.
  • Cell cycle analysis (e.g., flow cytometry) to determine cell cycle phase distribution after infection.

Main Results:

  • HHV-6A and HHV-6B induce the degradation of the Retinoblastoma protein (Rb), leading to the release of E2F1.
  • E2F1 and its cofactor DP1 are upregulated during HHV-6 infection, driving infected cells towards the S-phase.
  • Differential expression of E2F-responsive genes was observed in various cell types.
  • E2F binding sites were identified in the promoters of key HHV-6 genes (U27, U79), crucial for viral DNA replication.
  • Viral gene regulation by E2F1 synchronizes viral replication with the host cell cycle.
  • Roseolovirus infection results in cell cycle arrest, predominantly in the G2/M phase.

Conclusions:

  • E2F1 is a critical transcription factor for HHV-6 replication, enabling the virus to exploit the S-phase for DNA synthesis.
  • HHV-6 actively manipulates host cell cycle regulators to optimize conditions for viral replication.
  • The observed G2/M cell cycle arrest in roseolovirus infections suggests complex regulatory mechanisms influencing viral propagation.

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