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Department of Microbiology, Immunology, and Parasitology, LSU Medical Center, New Orleans, LA 70112
Dehydroepiandrosterone and androstenediol (AED) have previously
been found to protect mice from viral-induced encephalitis resulting in
an increased survival rate of the animals. These hormones have been
shown to antagonize corticosteroids, which have immunosuppressive
effects in vivo and in vitro, suggesting the antiviral effect of DHEA
and AED may be linked to the anticorticosteroid action. The present
study was undertaken to address the immune response to herpes simplex
virus type 1 (HSV-1) during the acute ocular infection with and without
AED treatment focusing on the early immune events in the eye and
trigeminal ganglion. AED treatment was found to significantly improve
the survival of HSV-1-infected mice in a dose-dependent fashion. While
AED did not antagonize the elevated serum corticosterone levels
following acute infection, AED enhanced the expression of IFN-
mRNA
and decreased the expression of HSV-1-infected cell polypeptide 27 mRNA
in the trigeminal ganglion during the acute (day 6 postinfection)
infection of mice, as determined by reverse transcription-PCR. However,
there was no change in the viral load from the eye or trigeminal
ganglion when comparing the AED-treated with the vehicle-treated mice.
Neutralization Abs to IFN-, -ß, or -/ß, but not control Ab,
blocked the protective effect following AED exposure, confirming the
involvement of type I IFN in the enhancement of survival in AED-treated
mice. Collectively, these results identify innate immunity as a key
component in augmenting the survival of HSV-1-infected mice following
AED treatment.
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