Neuropathol Appl Neurobiol. 2022 Jun 10:e12828. doi: 10.1111/nan.12828. Online ahead of print.
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 hybridization 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 2 regions were not statistically significant. In the cerebral cortex, Type 1 lesions overwhelmingly predominated, and only 14% Type 1 versus 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 days fever) and the “late” group (≥ 8 days 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.
PMID:35689364 | DOI:10.1111/nan.12828
