Project description:To explore the underlying mechanism of recurrent SARS-CoV-2 infection in convalescent patients. We performed single-cell RNA sequencing on peripheral blood mononuclear cells isolated from a recurrent patient, taking 14 recovered COVID-19 patients and 4 dead COVID-19 patients as controls.
Project description:Background: Acute kidney injury (AKI) is a common sequela of infection with SARS-CoV-2 and contributes to the severity and mortality from COVID-19. Here, we tested the hypothesis that kidney alterations induced by COVID-19-associated AKI could be detected in cells collected from urine. Methods: We performed single-cell RNA sequencing (scRNAseq) on cells recovered from the urine of eight hospitalized COVID-19 patients with (n=5) or without AKI (n=3) as well as four non-COVID-19 AKI patients (n=4) to assess differences in cellular composition and gene expression during AKI. Results: Analysis of 30,076 cells revealed a diverse array of cell types, most of which were kidney, urothelial, and immune cells. Pathway analysis of tubular cells from patients with AKI showed enrichment of transcripts associated with damage-related pathways compared to those without AKI. ACE2 and TMPRSS2 expression were highest in urothelial cells amongst cell types recovered. Notably, in one patient we detected SARS-CoV-2 viral RNA in urothelial cells. These same cells were enriched for transcripts associated with anti-viral and anti-inflammatory pathways. Conclusions: We successfully performed scRNAseq on urinary sediment from hospitalized patients with COVID-19 to noninvasively study cellular alterations associated with AKI and established a dataset that includes both injured and uninjured kidney cells. Additionally, we provide preliminary evidence of direct infection of urinary bladder cells by SARS-CoV-2. The urinary sediment contains a wealth of information and is a useful resource for studying the pathophysiology and cellular alterations that occur in kidney diseases.
Project description:As coronavirus disease 2019 (COVID-19) and aging are both accompanied by cognitive decline, we hypothesized that COVID-19 might lead to molecular signatures similar to aging. We performed whole-transcriptome analysis of the frontal cortex, a critical area for cognitive function, in individuals with COVID-19, age-matched and sex-matched uninfected controls, and uninfected individuals with intensive care unit/ventilator treatment. Our findings indicate that COVID-19 is associated with molecular signatures of brain aging and emphasize the value of neurological follow-up in recovered individuals.
Project description:Clinical outcomes of COVID-19 patients are worsened by the presence of co-morbidities, especially cancer for which mortality rate in cancer patients affected by COVID-19 is elevated. SARS-CoV-2 infection is known to alter immune system homeostasis. Whether cancer patients developing COVID-19 present alterations of immune functions which might contribute to worse outcomes has been so far poorly investigated. We conducted a multi-omic analysis of immunological parameters in COVID-19 patients with and without cancer. We found that 8 pro-inflammatory factors out of 27 analysed serum cytokines were modulated in COVID-19 patients irrespective of cancer status. Diverse subpopulations of T lymphocytes such as CD8+ T, CD4+ T central memory, Mucosal associated invariant T cells (MAIT) NKT and T cells were reduced while B memory cells, plasmablasts, late NK and plasmacytoid dendritic cells were expanded in COVID-19 cancer patients. A 19 gene expression signature of peripheral blood cells was able to discriminate COVID-19 cancer and without cancer patients. Gene set enrichment analysis highlights an increased gene expression in Interferon response and signalling which paired with aberrant cell cycle regulation in cancer patients. Ten out of these 19 genes were specific of COVID-19 cancer patients. Our findings illustrate a repertoire of aberrant alterations of gene expression in circulating immune cells of COVID-19 cancer patients that might contribute to decipher their higher frequency of severe events. We also unveil a transcriptional network involving gene regulators of both inflammation response and proliferation in PBMCs of COVID-19 cancer patients. This might also lead to design of novel therapeutic strategies for COVID-19 cancer patients.
Project description:Blood collected from recovered COVID-19 patients at 12, 16 and 24 weeks post infection was found to retain a signature of active infection which was associated with severity of disease
Project description:High-resolution mass spectrometry and the parallel quantitative evaluation of thousands of proteins has been used to characterise the proteomes of peripheral blood neutrophils from >200 individuals. This work has comprehensively mapped neutrophil molecular changes associated with mild versus severe COVID19 and identified significant quantitative changes in more than 1700 proteins in neutrophils from patients hospitalised with COVID19 versus patients with non-COVID19 acute respiratory infections. The study identifies neutrophil protein signatures associated with COVID19 disease severity. The data also show that alterations in neutrophil proteomes can persist in fully recovered patients and identify distinct neutrophil proteomes in recovered versus non recovered patients. Our study provides novel insights into neutrophil responses during acute COVID-19 and reveal that altered neutrophil phenotypes persist in convalescent COVID19 infections.
2022-08-17 | PXD036082 | Pride
Project description:Metagenome of elderly fatal and recovered COVID-19 patients
| PRJNA1049133 | ENA
Project description:Oral microbiome in patients with COVID-19