Coronavirus 2019:clinical and neuropathological aspects
Neurology
; 98(18 SUPPL), 2022.
Article
in English
| EMBASE | ID: covidwho-1925583
ABSTRACT
Objective:
To describe the clinicopathological correlations of 141 confirmed postmortem cases of coronavirus disease 2019 (COVID-19) due to severe acute respiratory syndrome-coronavirus -2 (SARS-CoV-2).Background:
Analysis of 50 cases of COVID-19 with available neuropathology revealed three CNS findings. First, hypoxia-ischemia does not account for all relevant neuropathological features. Second, elevated levels of circulating cytokines suggest activation of post-infectious immunity indicative of a cytokine storm, with increased hypercoagulability leading to a risk for thrombotic and hemorrhagic parenchymal tissue infarction. Third, a minority of cases have acute demyelinating encephalomyelitis-(ADEM) like features or indolent brainstem encephalitis. Such cases may present with early altered sensorium and brainstem signs. Fourth, SARS-CoV-2 staining could not be confirmed due to paucity of available tissue specimens. Design/Methods:
Ninety-four additional cases with available postmortem CNS neuropathology showed four additional findings.Results:
First, positive SARS-CoV-2 genome by PCR testing is present in brain tissues especially in olfactory bulb neurons and glial cells lending support to a route of entry into the CNS and the importance of early anosmia. Second, SARS-CoV-2-positive neurons appear to be TUNEL positive and caspase-positive, displaying reversible pT231 Tau localization in some cell soma that may be highly neurotoxic and a driver of tauopathy. Third, expression of ACE2 in oligodendrocytes is associated with viral entry, while TMPRSS2 and TMPRSS4 staining is implicated in pruning of viral-decorating spikes. Fourth, meningeal and interstitial brainstem inflammation by cytotoxic T-cells coincides with the localization of SARS-CoV-2 viral proteins in cranial nerves and interstitial areas of lower brainstem encephalitis. The detection of brain microglial activation and sparse perivascular and leptomeningeal T-cell infiltrates correlates with critical illness encephalopathy.Conclusions:
Genetic diversity, recombination, and viral mutation carries the foreseeable risk of continued fatality due to the direct and indirect effects of SARS-CoV-2 that include inflammatory vasculopathy, encephalitis, silent infarctions, and critical illness encephalopathy.
caspase; cytokine; endogenous compound; transmembrane protease serine 2; viral protein; anosmia; brain disease; brain stem; brain tissue; cell body; cell infiltration; central nervous system; clinical article; conference abstract; controlled study; coronavirus disease 2019; cranial nerve; critical illness; cytokine storm; cytotoxic T lymphocyte; encephalitis; encephalomyelitis; fatality; genetic variability; glia cell; human; human cell; human tissue; hypercoagulability; hypoxic ischemic encephalopathy; inflammation; nerve cell; neuropathology; neurotoxicity; nonhuman; olfactory bulb; oligodendroglia; parenchyma; polymerase chain reaction; protein expression; sensory system; Severe acute respiratory syndrome coronavirus 2; silent myocardial infarction; spike; T lymphocyte; tauopathy; thrombosis; TUNEL assay; vascular disease; virus entry
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Collection:
Databases of international organizations
Database:
EMBASE
Type of study:
Prognostic study
Language:
English
Journal:
Neurology
Year:
2022
Document Type:
Article
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