Reactivation of murine latent HSV infection by epinephrine iontophoresis

Insights

Epinephrine iontophoresis reactivated latent herpes simplex virus (HSV) in mice trigeminal ganglia, leading to ocular shedding. This method enables studying HSV latency, reactivation, and shedding.

Area of Science:

  • Ophthalmology
  • Virology
  • Neuroscience

Background:

  • Herpes simplex virus (HSV) establishes lifelong latency in trigeminal ganglia.
  • Reactivation of latent HSV can cause ocular disease.

Purpose of the Study:

  • To investigate the potential of epinephrine iontophoresis to induce HSV reactivation from latency.
  • To establish an ocular model for studying HSV latency and reactivation.

Main Methods:

  • BALB/c mice were infected with HSV-1 (strain McKrae) via corneal scarification.
  • Latent infection was established, followed by a 3-day epinephrine iontophoresis treatment.
  • Ocular shedding and trigeminal ganglia virus presence were monitored.

Main Results:

  • Epinephrine iontophoresis induced ocular HSV shedding in 70% of treated mice.
  • Infectious HSV was isolated from trigeminal ganglia of stimulated mice only.
  • Latent HSV was isolated from both stimulated and non-stimulated mice.

Conclusions:

  • Epinephrine iontophoresis is effective in reactivating latent HSV in the trigeminal ganglia.
  • This ocular model facilitates research into HSV latency, reactivation, and shedding.