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Host Immune Response to Enterovirus and Parechovirus Systemic Infections in Children
Anjana Sasidharan1, Wail M Hassan2, Christopher J Harrison1
1Department of Pathology and Laboratory Medicine, Children's Mercy Hospital and Clinics, Kansas City, Missouri, USA.
Insights
Enterovirus (EV) and parechovirus type A3 (PeV-A3) infections trigger distinct immune responses in children. EV causes robust cerebrospinal fluid (CSF) cytokine/chemokine release, while PeV-A3 elicits stronger plasma responses, potentially explaining clinical differences.
Area of Science:
- Pediatric infectious diseases
- Immunology
- Virology
Background:
- Enterovirus (EV) and parechovirus type A3 (PeV-A3) cause a spectrum of childhood infections.
- Understanding the innate immune response, particularly to PeV-A3, is crucial.
- This study investigates cytokine and chemokine profiles in children with EV and PeV-A3 infections.
Purpose of the Study:
- To compare cytokine and chemokine responses to Enterovirus and Parechovirus A3 infections in children.
- To analyze immune responses in both cerebrospinal fluid (CSF) and plasma.
- To correlate immune profiles with clinical presentations.
Main Methods:
- Analysis of 74 CSF and 35 paired plasma samples from children.
- Samples were categorized based on EV, PeV-A3, or no viral detection.
- Cytokine and chemokine levels were quantified using a 21-plex magnetic bead panel.
Main Results:
- Enterovirus (EV) induced significantly higher levels of fractalkine, IFN-α2, IFN-γ, IL-1Rα, IL-4, IL-8, and TNF-α in CSF.
- PeV-A3 elicited robust plasma responses with elevated IFN-α2, IL-15, IL-1Rα, IP-10, and MCP-1, but weaker CSF responses.
- Distinct cytokine/chemokine profiles were observed between EV and PeV-A3 infections.
Conclusions:
- Higher plasma cytokine/chemokine levels in PeV-A3 patients may correlate with prolonged fever.
- Lower PeV-A3 cytokine/chemokine levels in CSF could explain the absence of pleocytosis.
- Immune response patterns differ significantly between EV and PeV-A3 pediatric infections.
Background:
Enterovirus (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.
Methods:
A 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.
Results:
We 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.
Conclusions:
High 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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