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Journal of Clinical Microbiology, January 2000, p. 110-119, Vol. 38, No. 1
0095-1137/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
In Vitro and In Vivo Evaluations of Sodium Lauryl
Sulfate and Dextran Sulfate as Microbicides against Herpes Simplex and
Human Immunodeficiency Viruses
Jocelyne
Piret,1
Julie
Lamontagne,1
Julie
Bestman-Smith,1
Sylvie
Roy,1
Pierrette
Gourde,1
André
Désormeaux,1
Rabeea F.
Omar,1
Julianna
Juhász,2 and
Michel G.
Bergeron1,*
Centre de Recherche en
Infectiologie1 and Faculté de
Pharmacie,2 Université Laval, Ste-Foy,
Québec, Canada G1V 4G2
Received 1 June 1999/Returned for modification 21 September
1999/Accepted 8 October 1999
The efficacy of sodium lauryl sulfate (SLS), a sulfated anionic
chaotropic surfactant, and dextran sulfate (DS), a polysulfated carbohydrate, against herpes simplex virus (HSV) and human
immunodeficiency virus (HIV) infections was evaluated in cultured cells
and in different murine models of HSV infection. Results showed that both SLS and DS were potent inhibitors of the infectivities of various
HSV-1 and HSV-2 strains. Pretreatment of HIV-1 (strain NL4-3) with SLS
also reduced its infectivity to 1G5 cells. DS prevented the binding of
HSV to cell surface receptors and therefore its entry into cells.
Pretreatment of HSV-1 (strain F) with 50 µM SLS resulted in a
complete loss of virus infectivity to Vero cells. However, viruses were
able to enter into cells and to produce in the nuclei capsid shells
devoid of a DNA core. The amount of the glycoprotein D gene produced in
these cells remained unchanged compared to controls, suggesting that
SLS could interfere with the maturation of the virus. At a higher SLS
concentration (100 µM), HSV was highly damaged by SLS pretreatment
and only a few viral particles could enter into cells to produce
abnormal capsids. Although DS was a more potent inhibitor of HSV
infectivity in vitro, it was unable to provide any protection in murine
models of HSV infection. However, SLS conferred a complete protection of animals infected cutaneously with pretreated viruses. In addition, skin pretreatment of mice with a polymer formulation containing SLS
completely prevented the development of cutaneous lesions. More
interestingly, intravaginal pretreatment of mice with SLS in a buffered
solution also completely protected against lethal HSV-2 infection.
Taken together, our results suggest that SLS could thus represent a
candidate of choice as a microbicide to prevent the sexual transmission
of HIV, HSV, and possibly other pathogens that cause sexually
transmitted diseases.
*
Corresponding author. Mailing address: Centre de
Recherche en Infectiologie, RC 709, Centre Hospitalier Universitaire de
Québec, Pavillon CHUL, 2705 Boul. Laurier, Ste-Foy, Québec,
Canada G1V 4G2. Phone: (418) 654-2705. Fax: (418) 654-2715. E-mail:
Michel.G.Bergeron{at}crchul.ulaval.ca.
Journal of Clinical Microbiology, January 2000, p. 110-119, Vol. 38, No. 1
0095-1137/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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