Promyelocytic leukemia protein modulates establishment and maintenance of latent gammaherpesvirus infection in

Jaturong Sewatanon1, Hao Liu, Paul D Ling

  • 1Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.

Journal of Virology
|August 30, 2013
PubMed

Insights

Promyelocytic leukemia protein (PML) represses gammaherpesvirus latency. PML-deficient mice showed increased MHV68 reactivation and persistent infection, suggesting PML

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Promyelocytic leukemia protein (PML) organizes nuclear bodies (NBs) with antiviral functions.
  • Herpesviruses encode proteins to evade PML NB-mediated antiviral defenses.
  • In vivo studies on PML's role in herpesvirus infection are limited due to species specificity.

Purpose of the Study:

  • To investigate the in vivo effect of PML and PML NBs on gammaherpesvirus infection.
  • To elucidate PML's role in the establishment and maintenance of herpesvirus latency.

Main Methods:

  • Utilized wild-type and PML-deficient (PML⁻/⁻) mice.
  • Infected mice with murine gammaherpesvirus 68 (MHV68).
  • Analyzed acute infection, lytic reactivation, and persistent infection in peritoneal exudate cells.

Main Results:

  • Acute MHV68 infection progressed similarly in wild-type and PML⁻/⁻ mice.
  • PML⁻/⁻ mice exhibited higher lytic reactivation frequency in peritoneal cells.
  • Increased MHV68 genome-positive cells and enhanced reactivation efficiency were observed in PML⁻/⁻ mice.
  • A higher frequency of persistent infection was detected in PML⁻/⁻ peritoneal cells.

Conclusions:

  • PML protein can repress the establishment or maintenance of gammaherpesvirus latency in vivo.
  • The PML⁻/⁻ mouse model is valuable for dissecting molecular mechanisms of gammaherpesvirus latency.
  • Findings may provide insights into how PML modulates herpesvirus latency generally.

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