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<p>Nipah virus (NiV) is distributed in South-East Asia and the Western Pacific, with currently active outbreak sites. NiV causes an acute febrile illness with high mortality (40–70%), encephalitis, and long-term disability among survivors. Currently, there are no effective therapeutic or preventive interventions, and its potential for explosive spread resulted in its designation as a pathogen of international epidemiological concern. However, the pathophysiology of NiV-induced encephalitis remains unclear. Using a hamster model of NiV infection, we demonstrated that NiV targets several brain areas, such as the cortex and the hippocampus, infecting neurons, astrocytes, and blood-brain barrier cells. NiV infection also induced glial activation, including both microglia and astrocytes, leading to vascular and neuronal compromise and parenchymal lesions. Overall, NiV demonstrates a marked tropism for the central nervous system, resulting in major damage and death.</p>

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Nipah virus infects the brain and triggers neuronal and glial damage in a hamster model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月15日

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  • Karl Valerdi,
  • Takeshi Saito,
  • Ruchi Paroha,
  • Kirsten Littlefield,
  • Jessica Plante,
  • Kenneth Plante,
  • Silvana Valdebenito,
  • Junki Maruyama,
  • Eliseo Eugenin

摘要

Nipah virus (NiV) is distributed in South-East Asia and the Western Pacific, with currently active outbreak sites. NiV causes an acute febrile illness with high mortality (40–70%), encephalitis, and long-term disability among survivors. Currently, there are no effective therapeutic or preventive interventions, and its potential for explosive spread resulted in its designation as a pathogen of international epidemiological concern. However, the pathophysiology of NiV-induced encephalitis remains unclear. Using a hamster model of NiV infection, we demonstrated that NiV targets several brain areas, such as the cortex and the hippocampus, infecting neurons, astrocytes, and blood-brain barrier cells. NiV infection also induced glial activation, including both microglia and astrocytes, leading to vascular and neuronal compromise and parenchymal lesions. Overall, NiV demonstrates a marked tropism for the central nervous system, resulting in major damage and death.