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Low avidity T cell responses to SARS-CoV-2 in unexposed individuals and severe COVID-19

ABSTRACT: Low avidity T cell responses to SARS-CoV-2 in unexposed individuals and severe COVID-19

PROVIDER: PRJNA680539 | ENA |

REPOSITORIES: ENA

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Low avidity T cell responses to SARS-CoV-2 in unexposed individuals and severe COVID-19

Project description:Pre-existing memory T-cells against SARS-CoV-2 are present in a fraction of unexposed individuals and their induction by common cold corona viruses (CCCoVs) infection is suggested. Here we demonstrate that SARS-CoV-2-reactive T-cells were present in the memory compartment of virtually all unexposed individuals but possessed only low functional avidity. They harbored multiple, highly variable cross-reactivities that were not restricted to CCCoVs. Cross-reactivity to CCCoV was almost absent in COVID-19 patients. This was irrespective of strong T-cell memory against CCCoV in all donors. In severe but not mild COVID-19, SARS-CoV-2-specific T-cells also displayed low functional avidity and reduced clonal expansion, despite strongly increased frequencies. Our data question a major protective role of CCCoV for COVID-19. Instead, we suggest that a low avidity pre-existing T-cell memory may contribute to the excessive but low avidity T-cell responses, which we identified here as a hallmark of severe COVID-19.

2020-12-23 | GSE162086 | GEO

Low-Avidity CD4<sup>+</sup> T Cell Responses to SARS-CoV-2 in Unexposed Individuals and Humans with Severe COVID-19.

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Linear epitope-specific IgG responses to SARS-CoV-2 and related human coronaviruses in human COVID-19 convalescent sera

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CYP19A1 mediated sex hormone metabolism promotes severe disease outcome in SARS-CoV-2 infected male golden hamsters

Project description:Male sex belongs to one of the risk factors for severe COVID-19 outcome. However, underlying mechanisms that could affect sex dependent disease outcome are yet unknown. Here, we identified the CYP19A1 gene encoding for the testosterone-to-estradiol metabolizing enzyme CYP19A1 (alias aromatase) as a host factor that contributes to worsened disease outcome in male hamsters. SARS-CoV-2 infection increases CYP19A1 transcription most prominently in the lungs of male animals, which correlates with reduced circulating testosterone and increased circulating estradiol levels. Dysregulated sex hormone levels in male golden hamsters are associated with reduced lung function compared to females. Treatment of SARS-CoV-2 infected hamsters with letrozole, a clinically approved CYP19A1 inhibitor, supported recovery of dysregulated sex hormone levels and was associated with improved lung function in male but not female animals compared to placebo controls. Whole-lung transcriptome analysis in letrozole treated versus placebo treated control groups revealed key pathways associated with improved lung health in males. To seek translation of these findings into humans, we analyzed autopsy-derived lung samples of COVID-19 cases from three independent study sites. We found that CYP19A1 transcription and protein expression is strongly elevated in the lungs of men who died with COVID-19 as compared to females or non-COVID-19 controls. Our findings highlight the role of the lung as a yet unrecognized but critical organ involved in metabolic responses against respiratory virus infections. Furthermore, inhibition of CYP19A1 by the clinically approved drug letrozole may pose a new therapeutic strategy to reduce poor long-term COVID-19 outcome.

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In severe COVID-19, SARS-CoV-2 induces a chronic, TGF-β-dominated adaptive immune response (Activated B cells, Set 2)

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In severe COVID-19, SARS-CoV-2 induces a chronic, TGF-β-dominated adaptive immune response (Activated B cells, set 1)

Project description:Single cell transcriptome and BCR sequencing of FACS-sorted activated B cells of the peripheral blood of COVID-19 ICU patients and healthy controls

2021-02-09 | GSE158030 | GEO

Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals.

Project description: Not available

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