ArticleJournal of the neurological sciences2021
Detection of varicella zoster virus antigen and DNA in two cases of cerebral amyloid angiopathy.
Article in Journal of the neurological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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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.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Varicella zoster virus infection.Nature reviews. Disease primers · 2026Review
- Varicella zoster virus and the central nervous system.Nature reviews. Microbiology · 2026Review
- Herpes zoster and long-term risk of subjective cognitive decline.Alzheimer's research & therapy · 2024Article
- Immunohistochemical diagnosis of human infectious diseases: a review.Diagnostic pathology · 2022Review
- Targeted RNA Sequencing of VZV-Infected Brain Vascular Adventitial Fibroblasts Indicates That Amyloid May Be Involved in VZV Vasculopathy.Neurology(R) neuroimmunology & neuroinflammation · 2022Article
- Clinical characteristics and prognostic analysis of patients with herpesvirus meningitis/encephalitis based on cerebrospinal fluid mNGS positivity.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveVaricella zoster virus (VZV) vasculopathy and cerebral amyloid angiopathy (CAA) have similar clinical presentations: both affect cerebrovasculature in the elderly, produce hemorrhage, and can have a protracted course of cognitive decline and other neurological deficits. The cause of CAA is unknown, but amyloid-beta (Aβ) is found within arterial walls. Recent studies show that VZV induces Aβ and amylin expression and an amyloid-promoting environment. Thus, we determined if VZV was present in CAA-affected arteries.
methodsTwo subjects with pathologically-verified CAA were identified postmortem and frontal lobes analyzed by immunohistochemistry for arteries containing VZV, Aβ, and amylin and H&E for pathological changes. VZV antigen detection was confirmed by PCR for VZV DNA in the same region.
resultsIn both CAA cases, sections with cerebral arteries containing VZV antigen with corresponding VZV DNA were identified; VZV antigen co-localized with Aβ in media of arteries with histological changes characteristic of CAA. Amylin was also seen in the intima of a VZV-positive artery in the diabetic subject. Not all Aβ-containing arteries had VZV, but all VZV-positive arteries contained Aβ.
conclusionsVZV antigen co-localized with Aβ in some affected arteries from two CAA cases, suggesting a possible association between VZV infection and CAA.
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Registered trials
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