May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Butyrate Induces Ocular HSV–1 Shedding and Neuronal Reactivation in Mouse and Rabbit Eye Models
J.M. Hill; D.M. Neumann; D.T. Stark; L. Kodi; P.S. Bhattacharjee; H.W. Thompson; D.C. Bloom
Author Affiliations & Notes
  • J.M. Hill
    Ophthalmology, LSU Health Sciences Center, New Orleans, LA
  • D.M. Neumann
    Ophthalmology, LSU Health Sciences Center, New Orleans, LA
  • D.T. Stark
    Ophthalmology, LSU Health Sciences Center, New Orleans, LA
  • L. Kodi
    Ophthalmology, LSU Health Sciences Center, New Orleans, LA
  • P.S. Bhattacharjee
    Pathobiology, University of Guelph, Guelph, ON, Canada
  • H.W. Thompson
    Ophthalmology, LSU Health Sciences Center, New Orleans, LA
  • D.C. Bloom
    Molecular Genetics and Microbiology, University of Florida, Gainesville, FL
  • Footnotes
    Commercial Relationships  J.M. Hill, None; D.M. Neumann, None; D.T. Stark, None; L. Kodi, None; P.S. Bhattacharjee, None; H.W. Thompson, None; D.C. Bloom, None.
  • Footnotes
    Support  R01EY006311 (JMH), P30EY002377 (LSUEC core), F32EY016316 (DMN), R01AI048633 and BWF (DCB), RPB (JMH)
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 2802. doi:
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      J.M. Hill, D.M. Neumann, D.T. Stark, L. Kodi, P.S. Bhattacharjee, H.W. Thompson, D.C. Bloom; Butyrate Induces Ocular HSV–1 Shedding and Neuronal Reactivation in Mouse and Rabbit Eye Models . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2802.

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Abstract

Abstract: : Purpose.To determine if systemic administration of sodium butyrate, a known histone deacetylase inhibitor, induces HSV–1 ocular and neuronal reactivation in mice and rabbits latent with HSV–1. Methods: Mice (BALB/c females) were latently infected with HSV–1 strain McKrae (LAT+) or the LAT–negative control (dLAT2903). Rabbits (NZ white) were latently infected with HSV–1 strains McKrae or 17Syn+. Sodium butyrate (1.2 g/kg) was administered i.p. daily to mice on post inoculation (PI) days 28 and 29; eyes were swabbed on PI days 29 and 30 and trigeminal ganglia (TG) were obtained on day 30. Rabbits received butyrate in their drinking water (0.1%) and via daily i.p. injections (0.1 g/kg) for 22 days beginning on PI day 21; eyes were swabbed daily for 22 days beginning on day 21. Control rabbits received PBS. Results: Sodium butyrate–treated mice latent with McKrae (LAT+) showed high rates of reactivation (∼100%) as measured by the presence of infectious virus in tears and TG. Mice latent with HSV–1 recombinant dLAT2903 (LAT–) showed no reactivation. Rabbits treated with sodium butyrate had a significantly higher frequency of HSV–1 shedding (∼2–fold) and significantly more shedding episodes (∼2–fold) as measured by HSV–positive ocular swabs, compared with the PBS–treated rabbits. Conclusions: Butyrate induced HSV–1 reactivation in mice and rabbits latent with HSV–1 strains McKrae and 17Syn+. Our hypothesis is that LAT+ HSV–1 strains that are known to reactivate by adrenergic induction or immunosuppression will also reactivate when treated with butyrate. It is possible that chromatin remodeling augmented by the administration of butyrate is the mechanism of action of this drug in these animal models.

Keywords: herpes simplex virus • keratitis • pharmacology 
© 2005, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2024 Association for Research in Vision and Ophthalmology.
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