Open AccessNo evidence of aberrant amyloid β and phosphorylated tau expression in herpes simplex virus‐infected neurons of the trigeminal ganglia and brain
Author(s) -
Tran Dia.,
Bakx Amy T. C. M.,
Dis Vera,
Aronica Eleonora,
Verdijk Robert M.,
Ouwendijk Werner J. D.
Publication year - 2022
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/bpa.13044
Subject(s) - herpes simplex virus , phosphorylation , neuroscience , trigeminal ganglion , amyloid (mycology) , virology , amyloid β , pathology , biology , medicine , virus , microbiology and biotechnology , disease , sensory system
Increasing evidence supports the role of neurotropic herpes simplex virus 1 (HSV‐1) in the pathogenesis of Alzheimer's disease (AD). However, it is unclear whether previously reported findings in HSV‐1 cell culture and animal models can be translated to humans. Here, we analyzed clinical specimens from latently HSV‐1 infected individuals and individuals with lytic HSV infection of the brain (herpes simplex encephalitis; HSE). Latent HSV‐1 DNA load and latency‐associated transcript (LAT) expression were identical between trigeminal ganglia (TG) of AD patients and controls. Amyloid β (Aβ) and hyperphosphorylated tau (pTau) were not detected in latently HSV‐infected TG neurons. Aging‐related intraneuronal Aβ accumulations, neurofibrillary tangles (NFT), and/or extracellular Aβ plaques were observed in the brain of some HSE patients, but these were neither restricted to HSV‐infected neurons nor brain regions containing virus‐infected cells. Analysis of unique brain material from an AD patient with concurrent HSE showed that HSV‐infected cells frequently localized close to Aβ plaques and NFT, but were not associated with exacerbated AD‐related pathology. HSE‐associated neuroinflammation was not associated with specific Aβ or pTau phenotypes. Collectively, we observed that neither latent nor lytic HSV infection of human neurons is directly associated with aberrant Aβ or pTau protein expression in ganglia and brain.