Demonstrates neuronal and glial damage from Nipah virus infection in hamsters, indicating significant neurological risks.
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.
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Valerdi et al. (2026) studied this question.
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