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Role of mitochondria in parvovirus pathology

Jonna Nykky1, Matti Vuento1, Leona Gilbert1

  • 1Department of Biological and Environmental Science, and Nanoscience Center, University of Jyväskylä, Jyväskylä, Finland.

Plos One
|January 28, 2014
PubMed

Insights

Canine parvovirus (CPV) initially disrupts mitochondrial function but later causes significant damage, revealing insights into virus-mitochondria interactions and parvovirus pathology.

Area of Science:

  • Cell Biology
  • Virology
  • Mitochondrial Biology

Background:

  • Mitochondrial function is vital for cellular survival.
  • Viruses can disrupt mitochondrial functions.
  • The role of mitochondria in parvovirus-induced cell damage is not fully understood.

Purpose of the Study:

  • To investigate the association between canine parvovirus (CPV) and mitochondria.
  • To elucidate the impact of CPV infection on mitochondrial function and structure.

Main Methods:

  • Confocal microscopy
  • Electron microscopy
  • Measurement of mitochondrial transmembrane potential
  • Reactive oxygen species (ROS) detection
  • Analysis of ERK1/2 signaling pathway

Main Results:

  • CPV associates with the mitochondrial outer membrane early in infection.
  • Transient mitochondrial depolarization and increased ROS occur during viral entry, followed by normalization.
  • Cell survival signaling (ERK1/2) is activated early.
  • Significant mitochondrial damage and depolarization are observed at 12 hours post-infection, coinciding with viral non-structural protein 1 expression.

Conclusions:

  • CPV infection dynamically affects mitochondrial function, with an initial transient disruption followed by severe damage.
  • This study provides new insights into parvovirus pathology and the broader mechanisms of virus-mitochondria interactions.

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