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<p>Human bornavirus encephalitis (BVE) is a rare, emerging and fatal zoonotic disease mainly caused by the Borna disease virus 1 (BoDV-1), a non-cytolytic RNA virus. Despite increasing recognition, the immunopathogenesis of human BoDV-1 infection remains insufficiently characterised. Complete coronal and sagittal brain sections from four fatal BoDV-1 cases were analysed using digitised immunohistochemistry to quantify viral distribution and tissue responses. Transcriptome-based analyses characterised local immune cell profiles in relation to viral loads measured by RT-qPCR. BoDV-1 viral loads varied substantially between cases but showed region-specific enrichment in the basal ganglia and hippocampus, correlating with lymphocyte presence and reactive microglia and astrocytes. Immune cell deconvolution revealed viral load-dependent modulation dominated by innate immune and glial populations, including metabolic and reactive astrocyte states, IFNγ-responsive microglia, and dendritic cells, macrophages, neutrophils, basophils, and CD8⁺ T cells. This was accompanied by induction of interferon-stimulated genes, antigen presentation, protein synthesis, and oxidative stress pathways, with a transcriptional signature resembling non-lytic viral and autoimmune-like neuroinflammatory conditions rather than lytic infections. These findings support a model of BoDV-1 encephalitis characterised by a prominent innate immune response and comparatively limited adaptive immune signatures. This imbalance might potentially contribute to impaired viral clearance and extensive tissue damage, a possible relationship that warrants further investigation.</p>

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Multimodal profiling of immune responses reveals innate-adaptive immune imbalance in human bornavirus encephalitis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月14日

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  • Nicola Jungbäck,
  • Przemyslaw Grochowski,
  • Daniel Hieber,
  • Moritz Dinser,
  • Zuzanna Mielewczyk,
  • Thomas Pfefferkorn,
  • Birgit Muntau,
  • Thomas Richter,
  • Georg Rieder,
  • Antonios Bayas,
  • Klaus Hirschbühl,
  • Bruno Märkl,
  • Patrick Adam,
  • Dennis Tappe,
  • Friederike Liesche-Starnecker

摘要

Human bornavirus encephalitis (BVE) is a rare, emerging and fatal zoonotic disease mainly caused by the Borna disease virus 1 (BoDV-1), a non-cytolytic RNA virus. Despite increasing recognition, the immunopathogenesis of human BoDV-1 infection remains insufficiently characterised. Complete coronal and sagittal brain sections from four fatal BoDV-1 cases were analysed using digitised immunohistochemistry to quantify viral distribution and tissue responses. Transcriptome-based analyses characterised local immune cell profiles in relation to viral loads measured by RT-qPCR. BoDV-1 viral loads varied substantially between cases but showed region-specific enrichment in the basal ganglia and hippocampus, correlating with lymphocyte presence and reactive microglia and astrocytes. Immune cell deconvolution revealed viral load-dependent modulation dominated by innate immune and glial populations, including metabolic and reactive astrocyte states, IFNγ-responsive microglia, and dendritic cells, macrophages, neutrophils, basophils, and CD8⁺ T cells. This was accompanied by induction of interferon-stimulated genes, antigen presentation, protein synthesis, and oxidative stress pathways, with a transcriptional signature resembling non-lytic viral and autoimmune-like neuroinflammatory conditions rather than lytic infections. These findings support a model of BoDV-1 encephalitis characterised by a prominent innate immune response and comparatively limited adaptive immune signatures. This imbalance might potentially contribute to impaired viral clearance and extensive tissue damage, a possible relationship that warrants further investigation.