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Title: Neuronal infection is a major pathogenetic mechanism and cause of fatalities in human acute Nipah virus encephalitis
Authors: Ong, Kien Chai
Ng, Khong Ying
Ng, Chiu Wan
Tan, Soon Hao
Teo, Woon Li
Norain Karim
Kumar, Shalini
Wong, Kum Thong
Keywords: Nipah Virus
Acute Encephalitis
In Situ Hybridization
Issue Date: Oct-2022
Publisher: John Wiley and Sons Inc
Citation: Ong K. C., Ng, K. C., Ng, C. W., Tan, S. H., Teo, W. L., Norain Karim, Kumar, S., & Wong, K. T. (2022). Neuronal infection is a major pathogenetic mechanism and cause of fatalities in human acute Nipah virus encephalitis. Neuropathology and Applied Neurobiology, 48(6).
Abstract: Objectives: Acute Nipah (NiV) encephalitis is characterised by a dual pathogenetic mechanism of neuroglial infection and ischaemia-microinfarction associated with vasculitis-induced thrombotic occlusion. We investigated the contributions of these two mechanisms in fatal cases. Materials and methods: We analysed brain tissues (cerebrum, brainstem and cerebellum) from 15 autopsies using light microscopy, immunohistochemistry (IHC), in situ hybridisation and quantitative methods. Results: Three types of discrete plaque-like parenchymal lesions were identified: Type 1 with neuroglial IHC positivity for viral antigens and minimal or no necrosis; Type 2 with neuroglial immunopositivity and necrosis; and Type 3 with necrosis but no viral antigens. Most viral antigen/RNA-positive cells were neurons. Cerebral glial immunopositivity was rare, suggesting that microinfarction played a more important role in white matter injury. Type 1 lesions were also detected in the brainstem and cerebellum, but the differences between cerebral cortex and these two regions were not statistically significant. In the cerebral cortex, Type 1 lesions overwhelmingly predominated, and only 14% Type 1 vs 69% Type 2 lesions were associated with thrombosis. This suggests that neuronal infection as a mechanism of pathogenesis was more important than microinfarction, both in general and in Type 1 lesions in particular. Between the 'early' group (<8-day fever) and the 'late' group (≥8-day fever), there was a decrease of Type 1 and Type 2 lesions with a concomitant increase of Type 3 lesions, suggesting the latter possibly represented late-stage microinfarction and/or neuronal infection. Conclusion: Neuronal infection appears to play a more important role than vasculopathy-induced microinfarction in acute NiV encephalitis.
ISSN: 03051846
Appears in Collections:Journal Articles

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