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Spatial transcriptomics uncovers vasculature-centered cellular interactions driving Japanese encephalitis progression

Zhihua Ou^1,2,3, Zhaoyang Wang^4,5,6, Qi Chen^2,3,7

¹State Key Laboratory of Genome and Multi-omics Technologies, BGI Research, Shenzhen, China.

Nature Communications

|March 18, 2026

Summary

Japanese encephalitis virus (JEV) causes brain inflammation. Ly6c2+ monocytes carry the virus, while activated endothelial cells disrupt the blood-brain barrier, leading to cell death and disease progression.

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Area of Science:

Neurovirology
Immunology
Systems biology

Background:

Neuropathology mechanisms of neuroinvasive viruses are not fully understood.
Japanese encephalitis virus (JEV) is a significant cause of viral encephalitis globally.

Purpose of the Study:

To elucidate the cellular interactions driving Japanese encephalitis (JE) pathogenesis.
To create a spatiotemporal atlas of JE using advanced transcriptomic technology.

Main Methods:

Infection of BALB/c mice with JEV.
Application of Stereo-seq for in situ host and viral transcriptome analysis.
Construction of a comprehensive spatiotemporal atlas of JE pathogenesis.

Main Results:

Ly6c2+ monocytes identified as primary JEV carriers, abundant immune infiltrates, and IFN-γ sources in the brain.
Ackr1+ endothelial cell activation linked to blood-brain barrier disruption and monocyte recruitment.
Crosstalk between monocytes and endothelial cells orchestrates inflammation and cell death (pyroptosis, necroptosis).

Conclusions:

Targeting Ly6c2+ monocyte and Ackr1+ endothelial cell interactions may mitigate JE progression.
The study provides a framework for investigating other neurotropic viral diseases.
Understanding cellular crosstalk is key to combating neuroinvasive viral infections.