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Does herpes simplex virus establish latency in the eye of the mouse?

C M Claoué1, W A Blyth, T J Hill

  • 1University of Bristol, Department of Ophthalmology, Medical School.

Eye (London, England)
|January 1, 1987
PubMed

Insights

Herpes simplex virus (HSV) can establish latent infections in mouse trigeminal ganglia after ocular spread. The virus was reactivated from infected anterior eye segments, suggesting ocular latency is possible.

Area of Science:

  • Ophthalmology
  • Virology
  • Immunology

Background:

  • Herpes simplex virus (HSV) can cause ocular infections.
  • Zosteriform spread of HSV to the eye can lead to corneal scarring and neovascularization.
  • Latent HSV infection in the trigeminal ganglia is a known phenomenon.

Purpose of the Study:

  • To investigate the possibility of ocular latency of HSV in a mouse model.
  • To characterize the ocular pathology associated with HSV infection.
  • To determine if HSV can be reactivated from ocular tissues.

Main Methods:

  • Induction of zosteriform HSV spread to the mouse eye.
  • Histopathological examination of ocular tissues.
  • Viral isolation from eye washings, anterior segments, and trigeminal ganglia.
  • In vitro and organ culture of anterior eye segments.

Main Results:

  • Clinically scarred and neovascularized corneas with chronic inflammation and goblet cells were observed.
  • Latent HSV infection was confirmed in the trigeminal ganglia.
  • HSV was not isolated from eye washings but was recovered from anterior segments after in vitro culture.
  • HSV could be isolated from anterior segment halves after organ culture, but not immediately.

Conclusions:

  • Ocular HSV infection in mice can lead to significant corneal pathology.
  • Latent HSV infection within ocular tissues, specifically the anterior segment, is suggested.
  • The findings support the possibility of ocular latency, distinct from latency in the trigeminal ganglia.

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