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Cross talk between PML and p53 during poliovirus infection: implications for antiviral defense

Mathieu Pampin1, Yannick Simonin, Bruno Blondel

  • 1CNRS FRE 2944, Institut Lwoff, Villejuif, France.

Journal of Virology
|August 17, 2006
PubMed

Insights

Poliovirus infection activates the PML protein, recruiting p53 to nuclear bodies for antiviral defense. However, the virus degrades p53, hindering this protective response.

Area of Science:

  • Cell Biology
  • Virology
  • Immunology

Background:

  • PML nuclear bodies (NBs) are dynamic intranuclear structures crucial for antiviral defense.
  • PML protein, the organizer of NBs, is induced by interferon and plays a key role in host defense mechanisms.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which poliovirus infection triggers PML-dependent p53 activation.
  • To investigate the role of p53 in antiviral defense against poliovirus and how the virus circumvents this response.

Main Methods:

  • Studied molecular events following poliovirus infection in relation to PML and p53.
  • Utilized extracellular signal-regulated kinase (ERK) pathway analysis, SUMOylation assays, and protein localization studies.
  • Employed small interfering RNA (siRNA) for p53 knock-down and assessed poliovirus replication.
  • Investigated proteasome- and MDM2-dependent degradation pathways.

Main Results:

  • Poliovirus infection induces PML phosphorylation via ERK, increases PML SUMOylation, and relocates PML to the nuclear matrix.
  • These PML modifications recruit p53 to NBs, leading to p53 phosphorylation and activation of apoptosis-inducing genes.
  • p53 knock-down enhances poliovirus replication, confirming p53's role in antiviral defense, dependent on PML.
  • Poliovirus antagonizes p53's antiviral activity by inducing its proteasomal degradation, mediated by MDM2.

Conclusions:

  • Poliovirus infection manipulates PML and NBs to activate p53-mediated apoptosis as an initial antiviral defense.
  • The virus subsequently degrades p53 via the proteasome-MDM2 pathway to overcome this host defense and promote its replication.
  • Understanding this interplay is crucial for developing antiviral strategies targeting viral evasion mechanisms.

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