A human cerebral organoid model of West Nile virus encephalitis shows innate immunocompetency.

Overview

1. Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany
2. German Center for Infection Research (DZIF), Partner site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany
3. Faculty of Mathematics, Informatics and Natural Sciences, University of Hamburg, Hamburg, Germany

Abstract

West Nile virus (WNV), an arbovirus of emerging global interest, can cause neuroinvasive disease in humans. Currently, no protective vaccine or specific treatment is available for human WNV encephalitis. The virus induces neuronal cell death, while astrocytes and microglia cells are suspected to contribute to WNV pathology. Hence, understanding their role is crucial for future treatment approaches. In this study, we establish a WNV encephalitis model using human cerebral organoids, generated with male iPSCs. Infection results in heterogeneous kinetics with an early strong replication potentially leading to viral clearance, while a late peak was associated with more long-term infection. Viral foci are seen in cortical-like areas, rich in neurons and astrocytes, however void of microglia. Pro-inflammatory cytokines (IL-6, TNF-α, IL-18), chemokines (CXCL10, CCL17, CX3CL1, CCL2) and biomarkers (IL-1RA, sTREM-1, sRAGE, BDNF) are increasingly released. Conclusively, human cerebral organoids make suitable WNV encephalitis models with valuable properties to study acute and long-term infection.

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Code is available via Zenodo (10.5281/zenodo.18628798).

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Version 1, 30 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 4 authors, 2 keywords, 14 MeSH terms, 6 funders, 41 references.

Cite

This paper

Steffen, J. F., Widerspick, L., Jansen, S., & Tappe, D. (2026). A human cerebral organoid model of West Nile virus encephalitis shows innate immunocompetency. Nature communications, 17(1), 2318. https://doi.org/10.1038/s41467-026-70281-x

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