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Herpes simplex virus latency in human cornea

Y Shimomura1, Y Mori, Y Inoue

  • 1Department of Ophthalmology, Osaka University School of Medicine, Japan.

Japanese Journal of Ophthalmology
|January 1, 1993
PubMed
Summary
This summary is machine-generated.

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Herpes simplex virus type 1 (HSV-1) latency was investigated in corneas of patients with herpetic stromal keratitis. Latent HSV-1 was detected in corneal tissues, suggesting a potential role in recurrent herpetic keratitis.

Area of Science:

  • Ophthalmology
  • Virology
  • Immunology

Background:

  • Herpetic stromal keratitis is a significant cause of vision loss.
  • Recurrence of herpetic keratitis is often attributed to viral reactivation from latent herpes simplex virus type 1 (HSV-1).
  • The precise mechanisms triggering HSV-1 recurrence remain under investigation.

Purpose of the Study:

  • To investigate the presence and potential role of latent herpes simplex virus type 1 (HSV-1) in corneal tissue from patients with herpetic stromal keratitis.
  • To explore alternative theories for HSV-1 recurrence beyond the conventional ganglion trigger theory.

Main Methods:

  • Corneal tissues were obtained from 20 patients undergoing penetrating keratoplasty for herpetic stromal keratitis in the nonactive stage.
  • Corneal homogenization and centrifugation were performed to detect infectious virus in supernatants.

Related Experiment Videos

  • Cultured corneal sections were analyzed for the presence of latent HSV-1.
  • Main Results:

    • Infectious HSV-1 was not detected in the initial corneal supernatants.
    • Latent HSV-1 was successfully detected in cultured corneal sections from 8 out of 20 patients.
    • These findings suggest HSV-1 can remain latent within the cornea itself.

    Conclusions:

    • The cornea may serve as a site for latent herpes simplex virus type 1 (HSV-1) persistence.
    • Results support a revised 'ganglion and skin trigger theory,' where peripheral HSV-1 proliferation could stimulate ganglionic reactivation.
    • This challenges the sole reliance on the ganglion trigger theory for herpetic keratitis recurrence.