RT Journal Article
SR Electronic
T1 Alzheimer’s disease-associated β-Amyloid does not protect against Herpes Simplex Virus 1 brain infection
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.01.21.427570
DO 10.1101/2021.01.21.427570
A1 Olga Bocharova
A1 Kara Molesworth
A1 Narayan P. Pandit
A1 Ilia V. Baskakov
YR 2021
UL http://biorxiv.org/content/early/2021/01/22/2021.01.21.427570.abstract
AB Alzheimer’s 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 Aβ 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 Aβ plaques, only small, statistically non-significant protection against acute HSV-1 infection was observed, yet no colocalization between HSV-1 and Aβ plaques was found. While the current study questions the antiviral role of APP or Aβ, it neither supports nor refutes the viral etiology hypothesis of late-onset AD.Competing Interest StatementThe authors have declared no competing interest.