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The influence of calcium and reactive oxygen species on influenza virus-induced apoptosis

C W Olsen1, N Dybdahl-Sissoko, V S Hinshaw

  • 1Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison.

Cell Death and Differentiation
|April 1, 1996
PubMed

Insights

Avian influenza virus induces apoptosis in kidney cells, contrary to expectations. Calcium dysregulation promotes this cell death, while reactive oxygen species play a minimal role.

Area of Science:

  • Virology
  • Cell Biology
  • Apoptosis Research

Background:

  • Influenza A and B viruses induce apoptosis in Madin-Darby canine kidney (MDCK) cells.
  • Bcl-2 expression inhibits this virus-induced apoptosis.
  • Avian influenza virus A/Turkey/Ontario/7732/66 (H5N9) (Ty/Ont) is highly virulent.

Purpose of the Study:

  • To investigate the role of calcium (Ca2+) and reactive oxygen species (ROS) in Ty/Ont-induced apoptosis in MDCK cells.
  • To understand the mechanisms of apoptosis inhibition by bcl-2 in the context of influenza virus infection.

Main Methods:

  • Treatment of MDCK cells with Ca2+ chelators (EGTA, BAPTA-AM) and an ionophore (ionomycin).
  • Assessment of apoptosis induction and enhancement by Ty/Ont virus.
  • Evaluation of ROS involvement using antioxidants, hypoxia (N2 flushing), and nigericin.

Main Results:

  • Ca2+ chelators induced and enhanced Ty/Ont-induced apoptosis, an effect opposite to other apoptosis models.
  • Ionomycin blocked Ty/Ont-induced apoptosis.
  • Antioxidants, hypoxia, and nigericin did not inhibit Ty/Ont-induced apoptosis, suggesting ROS play a minor role.

Conclusions:

  • Reactive oxygen species likely play a minimal role in influenza virus-induced apoptosis in MDCK cells.
  • Calcium's influence on influenza-induced apoptosis is contrary to its role in other classical apoptosis models.

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