ArticleNeurology(R) neuroimmunology & neuroinflammation2017
Varicella zoster virus-infected cerebrovascular cells produce a proinflammatory environment.
Article in Neurology(R) neuroimmunology & neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Varicella zoster virus infection.Nature reviews. Disease primers · 2026Review
- Non-neuronal sites of latency for alphaherpesviruses.Journal of virology · 2026Review
- An explainable machine learning model predicts pediatric varicella encephalitis.Frontiers in cellular and infection microbiology · 2026Article
- Viral Infection and the Blood-Brain Barrier: Molecular Research Insights and Therapies.The Journal of infectious diseases · 2025Review
- A Diagnostic Approach to VZV Vasculopathy Using MR Vessel Wall Imaging.Internal medicine (Tokyo, Japan) · 2025Article
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Inhibitory effect of Alantolactone against varicella-zoster virus in vitro.Virology journal · 2025Article
- Ten Years ofNeurology(R) neuroimmunology & neuroinflammation · 2025Article
- Understanding the Mode of Action of Several Active Ingredients from the Micro-Immunotherapy Medicine 2LZONAJournal of inflammation research · 2025Article
- Prognostic factors associated with acute retinal necrosis treated non-surgically.Eye (London, England) · 2024Article
- Simian varicella virus infection and reactivation in rhesus macaques trigger cytokine and Aβ40/42 alterations in serum and cerebrospinal fluid.Journal of neurovirology · 2024Article
- Zoster-Associated Prothrombotic Plasma Exosomes and Increased Stroke Risk.The Journal of infectious diseases · 2023Article
- Article
- Recovery of intracranial stenoses in varicella zoster virus vasculitis after long-term treatment with valacyclovir and prednisolone.Neurological research and practice · 2022Article
- Targeted RNA Sequencing of VZV-Infected Brain Vascular Adventitial Fibroblasts Indicates That Amyloid May Be Involved in VZV Vasculopathy.Neurology(R) neuroimmunology & neuroinflammation · 2022Article
- Acute Stroke Caused by Progressive Intracranial Artery Stenosis Due to Varicella Zoster Virus Vasculopathy after Chemotherapy for Malignant Lymphoma.Internal medicine (Tokyo, Japan) · 2021Article
- Elevated serum substance P during simian varicella virus infection in rhesus macaques: implications for chronic inflammation and adverse cerebrovascular events.Journal of neurovirology · 2020Article
- Central nervous system infections produced by varicella zoster virus.Current opinion in infectious diseases · 2020Review
- Coordinated expression of vascular endothelial growth factor A and urokinase-type plasminogen activator contributes to classical swine fever virus Shimen infection in macrophages.BMC veterinary research · 2019Article
- Varicella Zoster Virus Induces Differential Cell-Type Specific Responses in Human Corneal Epithelial Cells and Keratocytes.Investigative ophthalmology & visual science · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo test whether varicella zoster virus (VZV) infection of human brain vascular cells and of lung fibroblasts directly increases proinflammatory cytokine levels, consistent with VZV as a causative agent in intracerebral VZV vasculopathy and giant-cell arteritis (GCA).
methodsConditioned supernatant from mock- and VZV-infected human brain vascular adventitial fibroblasts (HBVAFs), human perineurial cells (HPNCs), human brain vascular smooth muscle cells (HBVSMCs), and human fetal lung fibroblasts (HFLs) were collected at 72 hours postinfection and analyzed for levels of 30 proinflammatory cytokines using the Meso Scale Discovery Multiplex ELISA platform.
resultsCompared with mock infection, VZV infection led to significantly increased levels of the following: interleukin-8 (IL-8) in all cell lines examined; IL-6 in HBVAFs, HPNCs, and HFLs, with no change in HBVSMCs; and vascular endothelial growth factor A in HBVAFs, HBVSMCs, and HFLs, with a significant decrease in HPNCs. Other cytokines, including IL-2, IL-4, IL-15, IL-16, TGF-b, Eotaxin-1, Eotaxin-3, IP-10, MCP-1, and granulocyte macrophage colony-stimulating factor, were also significantly altered upon VZV infection in a cell type-specific manner.
conclusionsVZV infection of vascular cells can directly produce a proinflammatory environment that may potentially lead to prolonged arterial wall inflammation and vasculitis. The VZV-mediated increase in IL-8 and IL-6 is consistent with that seen in the CSF of patients with intracerebral VZV vasculopathy, and the VZV-mediated increase in IL-6 is consistent with the cytokine's elevated levels in temporal arteries and plasma of patients with GCA.
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.