Amyloid beta reduces cytopathic effects of Herpes Simplex virus type I

Alzheimer’s disease (AD) is a neurodegenerative disorder that is
characterized by memory loss and other types of dementia. Amyloid β (Aβ)
is a main cause of senile plaques detected in the brains of patients
with AD and other forms of dementia. Recent evidence suggests that the
buildup of Aβ is may be in response to microbial infections in the
central nervous system. Aβ has been shown to inhibit the growth of
bacteria and yeast; however, little work has tested its role in reducing
viral activity. The present work tests the hypothesis that Aβ
suppresses the cytopathic effects induced by the neurotropic Herpes
Simplex Virus Type I (HSV-1). To test this hypothesis, we treated
SH-SY5Y neuroblastoma cells with varying concentrations of Aβ one hour
before HSV-1 infection (1716 strain). Forty-eight hours after infection,
cell viability and morphology was assayed. First we determined cell
viability by utilizing the
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)
assay. The MTT assay indicated that pretreatment of Aβ (100nM, 1μM,
10μM) reduced HSV-1 induced cell death by 40% (p<0.01).
Photomicrographs of neuroblastoma cells infected with HSV-1
(multiplicity of infection; MOI=1) also demonstrated that Aβ
pretreatment reduced cytopathic effects of HSV-1. To more directly test
HSV-1 activity, plaque formation assays are ongoing. These data indicate
that the antimicrobial activities of Aβ are not limited to bacteria.
Overall, the results provide another link connecting HSV-1 infection and
the progression of AD.

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