Notch and Wnt signaling: mimicry and manipulation by gamma herpesviruses

S Diane Hayward1, Jianyong Liu, Masahiro Fujimuro

  • 1Viral Oncology Program, Sidney Kimmel Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA. dhayward@jhmi.edu

Insights

Gamma herpesviruses Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) hijack fundamental cell signaling pathways, Notch and Wnt. This manipulation aids viral replication and persistent infection by controlling host cell proliferation and differentiation.

Area of Science:

  • Cell biology
  • Virology
  • Molecular biology

Background:

  • Cell proliferation and differentiation are regulated by fundamental signaling pathways like Notch and Wnt.
  • Gamma herpesviruses, including EBV and KSHV, interact with and manipulate host cell pathways for their life cycle.
  • Viral replication and persistent infections are linked to the differentiation state of infected cells.

Purpose of the Study:

  • To review how gamma herpesviruses EBV and KSHV exploit Notch and Wnt signaling pathways.
  • To compare viral manipulation of these pathways with normal cellular signaling.

Main Methods:

  • Literature review of scientific articles on gamma herpesviruses, EBV, KSHV, Notch signaling, and Wnt signaling.
  • Comparative analysis of viral and cellular mechanisms within these pathways.

Main Results:

  • EBV and KSHV utilize Notch and Wnt pathways to promote viral gene expression, replication, and persistence.
  • Viral exploitation often involves subverting normal pathway functions to favor viral life cycle progression.
  • Specific interactions include influencing B cell proliferation for persistent infection.

Conclusions:

  • Gamma herpesviruses have evolved sophisticated mechanisms to co-opt cellular Notch and Wnt pathways.
  • Understanding these virus-pathway interactions is crucial for comprehending viral pathogenesis and developing therapeutic strategies.

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