ArticleBrain pathology (Zurich, Switzerland)2022
No evidence of aberrant amyloid β and phosphorylated tau expression in herpes simplex virus-infected neurons of the trigeminal ganglia and brain.
Article in Brain pathology (Zurich, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Acute viral encephalitis impacts dense-core amyloid plaque pathology and dysregulates myeloid responses to amyloid plaques.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Recent Insights into the Role of Herpesviridae in Alzheimer's Disease: A Structured Narrative Review Based on a Systematic Literature Search.Neurology international · 2026Review
- Varicella zoster virus and the central nervous system.Nature reviews. Microbiology · 2026Review
- Characterization of effects of a neurotropic murine coronavirus infection on Alzheimer's disease neuropathology of 5xFAD mice.bioRxiv : the preprint server for biology · 2026Article
- Herpes simplex virus-1 infection alters microtubule-associated protein Tau splicing and promotes Tau pathology in neural models of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- The Association Between Herpes Zoster, Antiherpetic Therapies, and Alzheimer's Disease: A Comprehensive Systematic Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Phosphorylated-tau associates with HSV-1 chromatin and correlates with nuclear speckles decondensation in low-density host chromatin regions.Neurobiology of disease · 2025Article
- Human herpesvirus 8 ORF57 protein is able to reduce TDP-43 pathology: network analysis identifies interacting pathways.Human molecular genetics · 2023Article
- Aβ plaques do not protect against HSV-1 infection in a mouse model of familial Alzheimer's disease, and HSV-1 does not induce Aβ pathology in a model of late onset Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2023Article
- No evidence of aberrant amyloid β and phosphorylated tau expression in herpes simplex virus-infected neurons of the trigeminal ganglia and brain.Brain pathology (Zurich, Switzerland) · 2022Article
- Role of Intracellular Amyloid β as Pathway Modulator, Biomarker, and Therapy Target.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.