Sodium lauryl sulfate increases the efficacy of a topical formulation of foscarnet against herpes simplex virus type 1 cutaneous lesions in mice

Citation
J. Piret et al., Sodium lauryl sulfate increases the efficacy of a topical formulation of foscarnet against herpes simplex virus type 1 cutaneous lesions in mice, ANTIM AG CH, 44(9), 2000, pp. 2263-2270
Citations number
60
Categorie Soggetti
Microbiology
Journal title
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
ISSN journal
00664804 → ACNP
Volume
44
Issue
9
Year of publication
2000
Pages
2263 - 2270
Database
ISI
SICI code
0066-4804(200009)44:9<2263:SLSITE>2.0.ZU;2-1
Abstract
The influence of sodium lauryl sulfate (SLS) on the efficacies of topical g el formulations of foscarnet against herpes simplex virus type 1 (HSV-1) cu taneous infection has been evaluated in mice. A single application of the g el formulation containing 3% foscarnet given 24 h postinfection exerted onl y a modest effect on the development of herpetic skin Lesions. Of prime int erest, the addition of 5% SLS to this gel formulation markedly reduced the mean lesion score. The improved efficacy of the foscarnet formulation conta ining SLS could be attributed to an increased penetration of the antiviral agent into the epidermis, In vitro, SLS decreased in a concentration-depend ent manner the infectivities of herpesviruses for Vero cells. SLS also inhi bited the HSV-1 strain F-induced cytopathic effect. Combinations of foscarn et and SLS resulted in subsynergistic to subantagonistic effects, depending on the concentration used. Foscarnet in phosphate-buffered saline decrease d in a dose-dependent manner the viability of cultured human skin fibroblas ts. This toxic effect was markedly decreased when foscarnet was incorporate d into the polymer matrix. The presence of SLS in the gel formulations did not alter the viabilities of these cells. The use of gel formulations conta ining foscarnet and SLS could represent an attractive approach to the treat ment of herpetic mucocntaneous lesions, especially those caused by acyclovi r-resistant strains.