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MYC Controls the Epstein-Barr Virus Lytic Switch.

Rui Guo1, Chang Jiang1, Yuchen Zhang2

  • 1Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Department of Microbiology, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.

Molecular Cell
|April 22, 2020
PubMed
Summary

Epstein-Barr virus (EBV) latency in B cells is maintained by MYC and associated factors repressing lytic reactivation. Decreased MYC levels during differentiation trigger EBV

Keywords:
DNA loopingMYCherpesviruslatency reversallytic reactivationtumor virus

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Area of Science:

  • Virology
  • Oncology
  • Immunology

Background:

  • Epstein-Barr virus (EBV) causes human malignancies and persists lifelong in memory B cells.
  • EBV maintains a latent state to evade immune detection, switching to a lytic program for replication.
  • Mechanisms maintaining EBV latency in tumors and B cells are not fully understood.

Purpose of the Study:

  • To identify host factors regulating Epstein-Barr virus (EBV) lytic reactivation.
  • To elucidate the role of MYC in controlling EBV latency and lytic replication.
  • To explore therapeutic targets for reversing EBV latency in Burkitt lymphoma.

Main Methods:

  • Genome-wide CRISPR/Cas9 screen in Burkitt lymphoma B cells.
  • Analysis of host factor networks repressing EBV lytic reactivation.
  • Investigation of MYC binding to the EBV genome and its effect on replication origins and promoters.

Main Results:

  • A network of host factors, including MYC, cohesins, FACT, STAGA, and Mediator, was identified that represses EBV lytic reactivation.
  • Depletion of MYC or its associated factors induced EBV lytic cycle reactivation in vitro and in Burkitt xenografts.
  • MYC directly binds the EBV lytic replication origin and suppresses its interaction with the BZLF1 promoter.
  • Decreased MYC levels correlate with plasma cell differentiation, a known trigger for EBV lytic reactivation.

Conclusions:

  • EBV utilizes MYC abundance as a sensor for B cell differentiation state to control its life cycle.
  • MYC and its associated host factors are critical for maintaining EBV latency.
  • Targeting MYC or its regulatory network offers a potential strategy for therapeutic reversal of EBV latency.