Publication details

Unraveling the role of human microglia in tick-borne encephalitis virus infection: insights into neuroinflammation and viral pathogenesis.

Authors

PRANCLOVA Veronika NEDVEDOVA Lenka KOTOUNOVA Eliska HÖNIG Vaclav DVORAKOVA Marketa DAVIDKOVA Marika BILY Tomas VANCOVA Marie RŮŽEK Daniel PALUS Martin

Year of publication 2024
Type Article in Periodical
Magazine / Source Microbes and Infection
MU Faculty or unit

Faculty of Science

Citation
web https://doi.org/10.1016/j.micinf.2024.105383
Doi https://doi.org/10.1016/j.micinf.2024.105383
Keywords Tick-borne encephalitis virus; Primary human microglia; Cytokine/chemokine; Neuroinflammation; Viral strains
Description Tick-borne encephalitis virus (TBEV) is a neurotropic orthoflavivirus responsible for severe infections of the central nervous system. Although neurons are predominantly targeted, specific involvement of microglia in pathogenesis of TBE is not yet fully understood. In this study, the susceptibility of human microglia to TBEV is investigated, focusing on productive infection and different immune responses of different viral strains. We investigated primary human microglia and two immortalized microglial cell lines exposed to three TBEV strains (Hypr, Neudörfl and 280), each differing in virulence. Our results show that all microglia cultures tested support long-term productive infections, regardless of the viral strain. In particular, immune response varied significantly with the viral strain, as shown by the differential secretion of cytokines and chemokines such as IP-10, MCP-1, IL-8 and IL-6, quantified using a Luminex 48-plex assay. The most virulent strain triggered the highest cytokine induction. Electron tomography revealed substantial ultrastructural changes in the infected microglia, despite the absence of cytopathic effects. These findings underscore the susceptibility of human microglia to TBEV and reveal strain-dependent variations in viral replication and immune responses, highlighting the complex role of microglia in TBEV-induced neuropathology and contribute to a deeper understanding of TBE pathogenesis and neuroinflammation.

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