Coxsackievirus B5 induced apoptosis of HeLa cells: effects on p53 and SUMO

Virology. 2010 Jan 20;396(2):256-63. doi: 10.1016/j.virol.2009.10.005. Epub 2009 Nov 10.

Abstract

Coxsackievirus B5 (CVB5), a human enterovirus of the family Picornaviridae, is a frequent cause of acute and chronic human diseases. The pathogenesis of enteroviral infections is not completely understood, and the fate of the CVB5-infected cell has a pivotal role in this process. We have investigated the CVB5-induced apoptosis of HeLa cells and found that it happens by the intrinsic pathway by a mechanism dependent on the ubiquitin-proteasome system, associated with nuclear aggregation of p53. Striking redistribution of both SUMO and UBC9 was noted at 4 h post-infection, simultaneously with a reduction in the levels of the ubiquitin-ligase HDM2. Taken together, these results suggest that CVB5 infection of HeLa cells elicit the intrinsic pathway of apoptosis by MDM2 degradation and p53 activation, destabilizing protein sumoylation, by a mechanism that is dependent on a functional ubiquitin-proteasome system.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis* / physiology
  • Cell Nucleus / physiology
  • Coxsackievirus Infections / virology*
  • Cytochromes c / metabolism
  • Enterovirus B, Human / physiology*
  • HeLa Cells / virology
  • Humans
  • Membrane Potential, Mitochondrial / physiology
  • Proteasome Endopeptidase Complex / physiology
  • SUMO-1 Protein / physiology*
  • Tumor Suppressor Protein p53 / physiology*
  • Ubiquitin-Conjugating Enzymes / physiology

Substances

  • SUMO-1 Protein
  • Tumor Suppressor Protein p53
  • Cytochromes c
  • Ubiquitin-Conjugating Enzymes
  • Proteasome Endopeptidase Complex
  • ubiquitin-conjugating enzyme UBC9