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bioRxiv · 10.1101/2021.01.21.427570

Alzheimer's disease-associated β-Amyloid does not protect against Herpes Simplex Virus 1 brain infection

Bocharova, O.·Molesworth, K.·Pandit, N. P.·Baskakov, I. V.
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Abstract

Alzheimers disease (AD) is devastating fatal neurodegenerative disease. An alternative to the amyloid cascade hypothesis is the hypothesis that a viral infection is key to the etiology of late-onset AD, with amyloid A{beta} peptides playing a protective role. Contrary to previous work, in the current study the 5XFAD genotype failed to protect mice against infection with two strains of herpes simplex virus 1 (HSV-1), 17syn+ and McKrae. Moreover, the region- or cell-specific tropisms of HSV-1 were not affected by the 5XFAD genotype, arguing that host-pathogen interactions were not altered. In aged 5XFAD mice with abundant A{beta} plaques, only small, statistically non-significant protection against acute HSV-1 infection was observed, yet no colocalization between HSV-1 and A{beta} plaques was found. While the current study questions the antiviral role of APP or A{beta}, it neither supports nor refutes the viral etiology hypothesis of late-onset AD.

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Bocharova, O., Molesworth, K., Pandit, N. P., Baskakov, I. V.. 2021-01-22. Alzheimer's disease-associated β-Amyloid does not protect against Herpes Simplex Virus 1 brain infection. https://doi.org/10.1101/2021.01.21.427570

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