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SARS-CoV-2-associated T-cell infiltration in the central nervous system

ABSTRACT: SARS-CoV-2-associated T-cell infiltration in the central nervous system

PROVIDER: PRJEB67800 | ENA |

REPOSITORIES: ENA

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Single-cell sequencing of glioblastoma reveals central nervous system susceptibility to SARS-CoV-2

Project description:Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the recent global COVID-19 outbreak, which led to a public health emergency. Entry of SARS-CoV-2 into human cells is dependent on the SARS-CoV receptor, angiotensin converting enzyme 2 (ACE2) receptor, and cathepsin. Cathepsin degrades the spike protein (S protein), which results in the entry of viral nucleic acid into the human host cell. Methods: We explored the susceptibility of the central nervous system (CNS) to SARS-CoV-2 infection using single-cell transcriptome analysis of glioblastoma. Results: The results showed that ACE2 expression is relatively high in endothelial cells (ECs), bone marrow mesenchymal stem cells (BMSCs), and neural precursor cells (NPCs). Cathepsin B (Cat B) and cathepsin (Cat L) were also strongly expressed in various cell clusters within the glioblastoma microenvironment. Immunofluorescence staining of glioma and normal brain tissue chips further confirmed that ACE2 expression co-localized with CD31, CD73, and nestin, which confirmed the susceptibility to SARS-CoV-2 of nervous system cells, including ECs, BMSCs and NPCs, from clinical specimens. Conclusions: These findings reveal the mechanism of SARS-CoV-2 neural invasion and suggest that special attention should be paid to SARS-CoV-2-infected patients with neural symptoms, especially those who suffered a glioma.

2020-11-12 | GSE157424 | GEO

Single-cell sequencing of glioblastoma reveals central nervous system susceptibility to SARS-CoV-2

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Iodine I 131 Monoclonal Antibody 3F8 in Treating Patients With Central Nervous System Cancer or Leptomeningeal Cancer

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SARS-CoV-2 Invades the Central Nervous System via the Olfactory Route in Rhesus Monkeys

Project description:Purpose: Neurological manifestations are frequently reported in the Coronavirus Disease 2019 (COVID-19) patients. However, the neuroinvasion mechanism of SARS-CoV-2 remains to be determined. In this study, we explored the neuroinvasion of SARS-CoV-2 via our established non-human primate (NHP) model of COVID-19. Single-cell sequencing was conducted to comprehensively determine effects of SARS-CoV-2 infection on the CNS in consideration of the its cellular heterogeneity. Methods: Rhesus monkeys (3-5 kg, 3-5years old) were used for this study. One monkey were intranasally infected with 1x 10^7 PFU of SARS-CoV-2 in 1mL of PBS, and another monkey was intracranially injected with 1x10^6 of SARS-CoV-2 in 200 µl of PBS. One monkey was intranasally and intracranially treated with PBS as a control. We analyzed the tissues collected on the 4 dpi and 7dpi following intranasal inoculation and on the 9 dpi following intracranial inoculation. Two thousand cells were used to create 5 different clusters, including microglia, mature neurons, oligodendrocytes, endothelial vascular cells, and astrocytes. Single-cell sequencing of were sequenced by an Illumina Novaseq6000 sequencer, the sequencing depth of each cell was at least 100,000 reads, and the paired-end 150 bp (PE150) reading strategy was adopted. Results and Conclusions: Single-cell sequencing data showed that mitochondrial-related genes ND3, ATP6 and COX3 were down-regulated in mature neurons, oligodendrocytes, endothelial vascular cells and microglia in the hippocampus, primary olfactory cortex, and cerebral cortex infected with SARS-CoV-2.

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SARS-CoV-2-associated T-cell infiltration in the central nervous system.

Project description:ObjectivesInfection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19). Although an acute SARS-CoV-2 infection mainly presents with respiratory illness, neurologic symptoms and sequelae are increasingly recognised in the long-term treatment of COVID-19 patients. The pathophysiology and the neuropathogenesis behind neurologic complications of COVID-19 remain poorly understood, but mounting evidence points to endothelial dysfunction either directly caused by viral infection or indirectly by inflammatory cytokines, followed by a local immune response that may include virus-specific T cells. However, the type and role of central nervous system-infiltrating T cells in COVID-19 are complex and not fully understood.MethodsWe analysed distinct anatomical brain regions of patients who had deceased as a result of COVID-19-associated pneumonia or complications thereof and performed T cell receptor Vβ repertoire sequencing. Clonotypes were analysed for SARS-CoV-2 association using public TCR repertoire data.ResultsOur descriptive study demonstrates that SARS-CoV-2-associated T cells are found in almost all brain areas of patients with fatal COVID-19 courses. The olfactory bulb, medulla and cerebellum were brain regions showing the most SARS-CoV-2 specific sequence patterns. Neuropathological workup demonstrated primary CD8+ T-cell infiltration with a perivascular infiltration pattern.ConclusionFuture research is needed to better define the relationship between T-cell infiltration and neurological symptoms and its long-term impact on patients' cognitive and mental health.

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Genomic profiling combined with gene expression profiling in primary central nervous system lymphoma

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