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Mitochondrial distribution and function in herpes simplex virus-infected cells.

T Murata1, F Goshima, T Daikoku

  • 1Laboratory of Virology, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.

The Journal of General Virology
|January 25, 2000
PubMed
Summary

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Herpes simplex virus (HSV) infection causes mitochondria to cluster around the nucleus with viral tegument proteins. This migration, dependent on microtubules, maintains mitochondrial function during early infection stages.

Area of Science:

  • Cell Biology
  • Virology
  • Mitochondrial Biology

Background:

  • Herpes simplex virus (HSV) is a human pathogen that can cause various infections.
  • Mitochondria play crucial roles in cellular energy production and apoptosis.
  • The interaction between viruses and host cell organelles like mitochondria is complex and not fully understood.

Purpose of the Study:

  • To investigate the behavior and function of mitochondria during HSV infection.
  • To determine the role of viral proteins in mitochondrial dynamics.
  • To elucidate the mechanism of mitochondrial migration in infected cells.

Main Methods:

  • Confocal microscopy to visualize mitochondria and viral proteins.
  • Western blotting to assess protein expression (cytochrome c oxidase subunit 2, HSP60).

Related Experiment Videos

  • Measurement of cellular ATP, lactate, and mitochondrial membrane potential.
  • Treatment with microtubule-disrupting agents (nocodazole, vinblastine).

    • Main Results:

    • Mitochondria migrated to the perinuclear region in HSV-infected cells.
    • HSV infection upregulated stress-responsive HSP60 but not cytochrome c oxidase subunit 2.
    • Cellular ATP, lactate, and mitochondrial membrane potential were maintained for at least 6 hours post-infection.
    • Viral tegument proteins (UL41, UL46) accumulated in the perinuclear region alongside mitochondria.
    • Mitochondrial clustering and protein accumulation were blocked by nocodazole and vinblastine, indicating microtubule dependence.

    Conclusions:

    • Mitochondria actively respond to HSV infection by migrating towards the nucleus.
    • This migration involves viral tegument proteins and relies on the microtubule cytoskeleton.
    • Mitochondrial function is preserved during the early to middle stages of HSV infection, suggesting a role in supporting viral replication.