Article ; Online: Neuronal infection is a major pathogenetic mechanism and cause of fatalities in human acute Nipah virus encephalitis.
Neuropathology and applied neurobiology
2022 Volume 48, Issue 6, Page(s) e12828
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 ... ...
| 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. |
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| MeSH term(s) | Encephalitis/pathology ; Henipavirus Infections/pathology ; Humans ; Immunohistochemistry ; Neurons/pathology |
| Language | English |
| Publishing date | 2022-06-18 |
| Publishing country | England |
| Document type | Journal Article ; Research Support, Non-U.S. Gov't |
| ZDB-ID | 80371-6 |
| ISSN | 1365-2990 ; 0305-1846 |
| ISSN (online) | 1365-2990 |
| ISSN | 0305-1846 |
| DOI | 10.1111/nan.12828 |
| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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