ArticleOpen forum infectious diseases2020
Host Immune Response to Enterovirus and Parechovirus Systemic Infections in Children.
Article in Open forum infectious diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Absent pleocytosis in infant viral central nervous system infections reflects lymphocyte depletion and cytokine activation.Nature communications · 2026Article
- Diagnosis, management, and outcomes of parechovirus infections in infants: an overview.Journal of clinical microbiology · 2024Review
- Parechovirus infection in human brain organoids: host innate inflammatory response and not neuro-infectivity correlates to neurologic disease.Nature communications · 2024Article
- Multivariate indicators of disease severity in COVID-19.Scientific reports · 2023Article
- Neurotropic EV71 causes encephalitis by engaging intracellular TLR9 to elicit neurotoxic IL12-p40-iNOS signaling.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEnterovirus (EV) and parechovirus type A3 (PeV-A3) cause infections ranging from asymptomatic to life-threatening. Host immune responses in children, particularly innate responses to PeV-A3, remain largely unknown. The aim of this study was to determine aspects of the cytokine/chemokine responses to EV and PeV-A3 in cerebrospinal fluid (CSF) and plasma obtained from children with systemic/central nervous system infection.
methodsA total of 74 salvaged CSF samples (27 with EV, 23 with PeV-A3, and 24 with neither EV nor PeV-A3) and 35 paired blood samples (10 with EV, 14 with PeV-A3, and 11 with neither) were studied. Concentrations of cytokines and chemokines were measured using a customized 21-plex MILLIPLEX MAP Human Cytokine/Chemokine Magnetic Bead Panel. Additionally, clinical characteristics data for all the patients were collected from electronic medical records to evaluate the potential association between the immune response and presentations.
resultsWe demonstrate that EV and PeV-A3 infections induce different cytokine/chemokine immune responses in children. EV induces more robust responses in CSF with significantly elevated levels of fractalkine, interferon (IFN)-α2, IFN-γ, interleukin (IL)-1Rα, IL-4, IL-8, and tumor necrosis factor α; PeV-A3 induces less robust or absent responses in CSF but robust responses in plasma, with significantly higher concentrations of IFN-α2, IL-15, IL-1Rα, interferon-γ-inducible protein-10, and monocyte chemoattractant protein-1.
conclusionsHigh cytokine/chemokine concentrations in the plasma of PeV-A3 patients compared with EV patients could explain higher/more prolonged fever in PeV-A3 patients, whereas relatively low cytokine/chemokine concentrations in PeV-A3 CSF might explain the absence of CSF pleocytosis.
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