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Differentiation-Dependent KLF4 Expression Promotes Lytic Epstein-Barr Virus Infection in Epithelial Cells.

Dhananjay M Nawandar1, Anqi Wang1, Kathleen Makielski2

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The transcription factor KLF4 drives Epstein-Barr virus (EBV) lytic infection in oral epithelial cells by activating viral gene promoters. This discovery explains how EBV establishes lytic infection in specific cell types.

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Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Epstein-Barr virus (EBV) causes B-cell and epithelial malignancies.
  • EBV lytically infects oral epithelial cells, leading to oral hairy leukoplakia (OHL) in immunosuppressed individuals.
  • The cellular mechanisms driving EBV's exclusive lytic infection in oral epithelial cells remain unclear.

Purpose of the Study:

  • To elucidate the cellular mechanisms governing EBV's lytic infection in differentiated oral epithelial cells.
  • To identify cellular factors that induce EBV reactivation in epithelial cells.

Main Methods:

  • Investigated the role of the transcription factor KLF4 in EBV infection.
  • Utilized telomerase-immortalized normal oral keratinocyte (NOK) cells in organotypic raft culture.
  • Assessed viral reactivation in response to chemical inducers and KLF4/BLIMP1 expression levels.
  • Examined KLF4 and BLIMP1 expression in normal oral tissue and OHL lesions.

Main Results:

  • KLF4 directly activates EBV immediate-early gene promoters (BZLF1 and BRLF1), inducing differentiation-dependent lytic infection.
  • EBV reactivation in NOK cells was localized to differentiated cell layers.
  • Endogenous KLF4 is essential for efficient lytic reactivation induced by phorbol ester and sodium butyrate.
  • KLF4 and BLIMP1 act synergistically to promote lytic EBV infection, with both factors expressed in differentiated epithelial cells and OHL lesions.

Conclusions:

  • KLF4 is a key cellular factor inducing differentiation-dependent lytic EBV infection in epithelial cells.
  • KLF4, in conjunction with BLIMP1, plays a critical role in mediating EBV lytic reactivation in the oral epithelium.
  • This finding provides insight into EBV pathogenesis and potential therapeutic targets.