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Published on: August 15, 2019
Clinical, laboratory and immune aspects of Zika virus-associated encephalitis in children
Doris M Salgado1, Rocío Vega1, Jairo Antonio Rodríguez1
1Programa de Medicina, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia; Departamento de Pediatría, Hospital Universitario de Neiva, Neiva, Huila, Colombia; Especialización Médica en Pediatría, Postgrados Clínicos, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia.
Insights
Zika virus (ZIKV) caused pediatric encephalitis in Colombia, with faster symptom resolution than other causes. The virus triggered localized cytokine responses in the central nervous system, not systemic inflammation.
Area of Science:
- Neuroscience
- Virology
- Immunology
Background:
- Zika virus (ZIKV) outbreaks have been linked to neurological complications, including encephalitis.
- Pediatric encephalitis poses a significant public health challenge, necessitating understanding of its diverse etiologies.
Purpose of the Study:
- To investigate the clinical, laboratory, and immune characteristics of ZIKV-associated encephalitis in children.
- To differentiate ZIKV encephalitis from other causes of pediatric encephalitis in southern Colombia.
Main Methods:
- A pediatric neuro-surveillance study was conducted over one year in Colombia.
- Encephalitis cases were confirmed using molecular and serological tests in CSF, plasma, and urine.
- Cytokine levels (IL-10, IL-2, IL-4, IL-6, IFN-γ, TNF-α) were measured using flow cytometry.
Main Results:
- Six out of 16 confirmed encephalitis cases were associated with ZIKV infection; others were bacterial or caused by herpes viruses, enterovirus, or dengue virus type 2.
- ZIKV-associated encephalitis patients showed faster symptom resolution and lymphocytic pleocytosis in CSF.
- Elevated IL-6, IL-10, and IFN-γ were found in CSF, but not plasma, in a ZIKV-positive patient, suggesting localized immune response.
Conclusions:
- ZIKV is a significant cause of pediatric encephalitis in endemic regions.
- ZIKV infection appears to induce localized cytokine expression within the central nervous system rather than a systemic inflammatory response.
Objective:
To evaluate the clinical, laboratory, and immune characteristics of Zika virus (ZIKV)-associated encephalitis in pediatric patients after the epidemic in Huila, southern Colombia.
Methods:
A pediatric neuro-surveillance hospital study was conducted in a referral health center in southern Colombia, from October 2016 to October 2017. Cases of encephalitis were confirmed by nucleic acid amplification tests and serological methods in cerebrospinal fluid (CSF), plasma, and/or urine. Levels of six cytokines were evaluated by flow cytometry. Patients underwent daily clinical and laboratory follow-up.
Results:
Twenty children with probable encephalitis were included for further studies and 16 of them were confirmed. Four cases of bacterial meningoencephalitis (Streptococcus pneumoniae, group B Streptococcus, Staphylococcus epidermidis, and Escherichia coli) and 12 cases of viral encephalitis were identified, six of them associated with ZIKV infection. Other viral encephalitis cases were caused by herpes viruses (n=3), enterovirus (n=2), and dengue virus type 2 (DENV-2; n=1) infections. ZIKV-associated encephalitis symptoms subsided faster than those of patients with encephalitis caused by other agents. CSF analysis revealed lymphocytic pleocytosis. Compared to healthy controls, children with ZIKV-associated encephalitis presented modest plasma interleukin (IL)-10 but not IL-2, IL-4, IL-6, interferon gamma (IFN-γ), or tumor necrosis factor alpha (TNF-α). Cytokine expression was differentially regulated, as dramatically elevated IL-6, IL-10, and IFN-γ levels were observed in CSF but not in paired plasma samples in one of the patients with ZIKV detectable in CSF.
Conclusions:
This study provides evidence that ZIKV is responsible for pediatric encephalitis in endemic areas, and the local presence of the virus may induce cephalic but not systemic expression of cytokines.
