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Mitochondrial bioenergy alterations in avian HD11 macrophages infected with infectious bronchitis virus

Sergio E L da Silva1, Helena L Ferreira2, Andrea F Garcia3

  • 1Faculdade de Medicina Veterinária (FAMEV), Universidade Federal Uberlândia (UFU), Uberlândia, MG, Brazil.

Archives of Virology
|January 6, 2018
PubMed

Insights

Infectious bronchitis virus (IBV) causes cell damage and apoptosis in avian macrophages by disrupting mitochondrial function and increasing reactive oxygen species (ROS). This mitochondrial dysfunction occurs without hindering viral replication.

Area of Science:

  • Avian immunology
  • Virology
  • Cell biology

Background:

  • Infectious bronchitis virus (IBV) is a significant pathogen in poultry.
  • Mitochondrial dysfunction is implicated in various cellular stress responses.
  • Apoptosis, or programmed cell death, is a critical cellular process.

Purpose of the Study:

  • To investigate the link between mitochondrial dysfunction and apoptosis in avian macrophages infected with IBV.
  • To characterize the effects of IBV M41 strain on HD11 cells.

Main Methods:

  • HD11 avian macrophage cells were infected with the IBV M41 strain.
  • Cellular effects, apoptosis, mitochondrial membrane potential, and ROS production were assessed at various time points post-infection.

Main Results:

  • IBV M41 infection induced cytopathic effects and viral particle release.
  • Apoptotic cell numbers increased significantly at 24, 48, and 72 hours post-infection.
  • Mitochondrial membrane depolarization and ROS production were observed throughout the infection period.

Conclusions:

  • IBV M41 replication in macrophages leads to mitochondrial bioenergetic failure.
  • Mitochondrial dysfunction acts as a respiratory chain uncoupler during IBV infection.
  • Viral replication proceeds effectively despite induced mitochondrial dysfunction.

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