J. Bestman-smith et al., Sodium lauryl sulfate abrogates human immunodeficiency virus infectivity by affecting viral attachment, ANTIM AG CH, 45(8), 2001, pp. 2229-2237
The microbicidal activity of sodium lauryl sulfate (SLS) against human immu
nodeficiency virus type 1 (HIV-1) was studied in cultured cells. Pretreatme
nt of HIV-1(NL4-3) with SLS decreased, in a concentration-dependent manner,
its infectivity when using 1G5 as target cells. In the absence of a viral
pretreatment period or when 1G5 cells were pretreated with SLS, the surfact
ant-induced inactivation of viral infectivity was less pronounced, especial
ly at concentrations between 375 and 550 muM. SLS had no effect on HIV-1 wh
en the virus was adsorbed to 1G5 cells by a 2-h incubation period. SLS almo
st completely inhibited the fusion process by decreasing the attachment of
HIV-1 to target cells. SLS also inhibited the infectivity of HIV-1-based lu
ciferase reporter viruses pseudotyped with the amphotropic murine leukemia
virus envelope ( which enters cells in a CD4-, CCR5-, and CXCR4-independent
manner), indicating that SLS may inactivate other envelope viruses. In con
trast, no effect was seen with vesicular stomatitis virus envelope glycopro
tein G (which enters cells through receptor-mediated endocytosis) pretreate
d with up to 700 muM SLS. SLS also decreased, in a dose-dependent manner, t
he HIV-1-dependent syncytium formation between 1G5 and J1.1 cells after a 2
4-h incubation. The reduction of luciferase activity was more pronounced wh
en J1.1 cells (which express HIV-1 proteins on their surface) were pretreat
ed with SLS rather than 1G5 cells. Taken together, our results suggest that
SLS could represent a candidate of choice for use in vaginal microbicides
to prevent the sexual transmission of HIV and possibly other pathogens caus
ing sexually transmitted diseases.