title: Valacyclovir inhibits recovery of ocular HSV-1 after experimental reactivation by excimer laser keratectomy.
abstract: OBJECTIVE
  The goal of this was to determine whether the systemic administration of valacyclovir (Valtrex) would reduce ocular shedding of herpes simplex virus 1 (HSV-1) after excimer laser ablation in the New Zealand rabbit latency model.
  
  
  METHODS
  The in vitro 50% inhibitory concentration (IC50) of HSV-1 W strain was determined by using a plaque-reduction assay to verify its sensitivity to acyclovir. Forty-seven NZW rabbits latently infected with HSV-1 W strain were divided into four groups: I, 50 mg/kg/day valacyclovir; II, 100 mg/kg/day valacyclovir; III, 150 mg/kg/day valacyclovir; and IV, saline control. One half of the total dose of valacyclovir was delivered via intraperitoneal injections twice daily for 7 days beginning with one dose before excimer laser keratectomy. HSV-1 ocular shedding was determined from eye cultures for 7 days after treatment.
  
  
  RESULTS
  The IC50 for HSV-1 W was determined to be 2.9 microg/ml. The administration of both 100 mg/kg/day (group II) and 150 mg/kg/day (group III) of valacyclovir significantly reduced the number of eyes from which latent HSV-1 was recovered compared with the control group. There was no difference between the control group and group I (50 mg/kg/day valacyclovir). However, all three valacyclovir dosages significantly reduced the total number of HSV-1 shedding days compared with the control group, and 100% HSV-1 TG latency was demonstrated for all four groups.
  
  
  CONCLUSIONS
  Systemic administration of valacyclovir significantly reduced HSV-1 ocular shedding in a dose-dependent manner after excimer laser keratectomy in the NZW rabbit latency model.
authors.affiliation: Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania 15203, USA. dhaliwal@vision.eei.upmc.edu
authors.forename: D K
authors.initials: DK
authors.lastname: Dhaliwal
authors.forename: E G
authors.initials: EG
authors.lastname: Romanowski
authors.forename: K A
authors.initials: KA
authors.lastname: Yates
authors.forename: D A
authors.initials: DA
authors.lastname: Barnhorst
authors.forename: M
authors.initials: M
authors.lastname: Goldstein
authors.forename: R G
authors.initials: RG
authors.lastname: Deeter
authors.forename: D N
authors.initials: DN
authors.lastname: Fish
authors.forename: Y J
authors.initials: YJ
authors.lastname: Gordon
mesh_terms: D000212:Acyclovir / Q000031:analogs & derivatives* / Q000097:blood / Q000494:pharmacology; D000818:Animals; D000998:Antiviral Agents / Q000097:blood / Q000494:pharmacology*; D003315:Cornea / Q000601:surgery*; D005123:Eye / Q000821:virology*; D005260:Female; D018259:Herpesvirus 1, Human / Q000187:drug effects* / Q000254:growth & development*; D020128:Inhibitory Concentration 50; D053685:Laser Therapy; D011817:Rabbits; D012668:Trigeminal Ganglion / Q000821:virology; D000077483:Valacyclovir; D014633:Valine / Q000031:analogs & derivatives* / Q000097:blood / Q000494:pharmacology; D014775:Virus Activation; D017735:Virus Latency; D017201:Virus Shedding / Q000187:drug effects
chemical_list: D000998:Antiviral Agents; D014633:Valine; D000077483:Valacyclovir; D000212:Acyclovir