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Promyelocytic leukemia-nuclear body proteins: herpesvirus enemies, accomplices, or both?

Ryan T Saffert1, Robert F Kalejta

  • 1University of Wisconsin-Madison, Institute for Molecular Virology & McArdle Laboratory for Cancer Research, Madison, WI, USA Tel.: +1 608 265 5546; ; rtsaffert@wisc.edu.

Future Virology
|September 19, 2009
PubMed

Insights

PML-nuclear bodies (PML-NBs) play a dual role in herpesvirus replication. These structures inhibit lytic replication but enhance latent infections, depending on the cell type and viral lifecycle stage.

Area of Science:

  • Cellular biology
  • Virology
  • Subnuclear structures

Background:

  • Promyelocytic leukemia (PML) protein forms PML-nuclear bodies (PML-NBs) with proteins like Daxx and Sp100.
  • PML-NBs are sites where viral genomes often localize, prompting research into their role in viral replication.
  • Viral proteins can modify or disrupt PML-NBs, creating a debate about their overall effect on viral replication.

Purpose of the Study:

  • To review and discuss recent data on the role of PML-NBs in herpesvirus replication.
  • To clarify whether PML-NBs inhibit or enhance viral replication.
  • To examine the context-dependent function of PML-NBs in different herpesvirus infection stages.

Main Methods:

  • Literature review and data synthesis.
  • Analysis of studies investigating herpesvirus interactions with PML-NBs.
  • Comparative analysis of PML-NB function in lytic versus latent infections.

Main Results:

  • PML-NB proteins inhibit herpesvirus replication in cell types supporting productive, lytic infection.
  • PML-NB proteins enhance the establishment of lifelong latent herpesvirus infections in other cell types.
  • The function of PML-NBs in viral replication is cell-type and infection-stage dependent.

Conclusions:

  • PML-NBs exhibit opposing roles in herpesvirus replication, inhibiting lytic cycles while promoting latency.
  • Understanding the dual role of PML-NBs is crucial for comprehending herpesvirus lifecycle and pathogenesis.
  • Further research is warranted to elucidate the precise mechanisms underlying PML-NBs' context-specific functions in viral infections.

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