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Cyclooxygenase (COX)-inhibiting drug reduces HSV-1 reactivation in the mouse eye model

Shiro Higaki1, Keizo Watanabe, Motoki Itahashi

  • 1Department of Ophthalmology, Kinki University School of Medicine, Osaka-Sayama, Japan. higaki@ganka.med.kindai.ac.jp

Current Eye Research
|March 11, 2009
PubMed
Abstract

Insights

Bromfenac sodium eye drops showed potential in suppressing herpes simplex virus type 1 (HSV-1) reactivation in a mouse model. Further research is needed to confirm its efficacy in clinical settings.

Area of Science:

  • Ophthalmology
  • Virology
  • Pharmacology

Background:

  • Herpes simplex virus type 1 (HSV-1) establishes lifelong latency in sensory neurons.
  • Reactivation of HSV-1 can lead to ocular disease, including herpetic keratitis.
  • Cyclooxygenase (COX) inhibitors are explored for their potential antiviral properties.

Purpose of the Study:

  • To investigate the efficacy of COX inhibitors in suppressing HSV-1 reactivation.
  • To evaluate bromfenac sodium, pranoprofen, and etodolac for their ability to prevent HSV-1 recurrence in a mouse model.

Main Methods:

  • BALB/c mice with latent HSV-1 infection were treated with bromfenac sodium, pranoprofen, etodolac, or saline eye drops.
  • Latent HSV-1 was reactivated, and ocular surface swabs were cultured for infectious virus.
  • Viral loads in eyes and trigeminal ganglia (TGs) were quantified using real-time PCR.

Main Results:

  • Bromfenac sodium eye drops demonstrated a statistically significant reduction in positive HSV-1 swab results compared to saline (p = 0.033).
  • No significant differences in viral DNA levels were observed in the eyes or TGs among the drug-treated groups and the saline control group.
  • Pranoprofen and etodolac did not show significant suppression of HSV-1 reactivation compared to the saline group.

Conclusions:

  • Bromfenac sodium eye drops exhibit potential in suppressing HSV-1 reactivation.
  • Current COX inhibitors tested did not significantly reduce viral loads in ocular tissues or TGs during reactivation.
  • Further studies are warranted to elucidate the precise mechanisms and clinical applicability of bromfenac sodium for HSV-1 suppression.

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