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Determination of immunological deviations in post-COVID-19 syndromes by single cell omics

Subject Area General Genetics and Functional Genome Biology
Clinical Infectiology and Tropical Medicine
Term from 2021 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 466168337
 
Final Report Year 2025

Final Report Abstract

Long COVID (LC19) is a complex syndrome that occurs in many people worldwide after a SARS-CoV-2 infection. The causes and underlying mechanisms are diverse and have not yet been conclusively clarified. The first cases of LC19 were documented in the first year of the pandemic, which led to the application for this research project at the end of 2020. Approval was granted at the beginning of 2021 and the project started in the summer of the same year. As part of the German COVID-19 Omics Initiative (DeCOI), we had already been able to show in the first year of the pandemic that the pathology of acute COVID disease can be characterized particularly well using single-cell genomics. Together with L-E. Sander (Charité we (Aschenbrenner, Schultze) contacted C. Scheibenbogen (Charité) back then, who dealt with patients who developed LC19 symptoms after acute SARS-CoV-2 infection at an early stage. Since we had to assume that LC19 would be extremely heterogeneous as a clinical picture, we decided in the course of the project to focus on patients who had reported only mild symptoms during the acute phase of COVID disease and were not hospitalized. A total of 40 patients were included in the study and compared with 20 patients who had reported a similarly mild course of COVID disease but did not suffer from LC19. PBMCs were isolated from all patients and single-cell transcriptomes were generated. In addition to the direct measurements of PBMC from peripheral blood, we also performed ex vivo stimulations with known stimulators of the innate and adaptive immune system (CytoStim, Poly I:C, R848) and the spike protein of SARS-CoV-2 and compared the reactivity of the peripheral immune system in both patient groups. Four of the five questions posed in the application were answered by the project. The question of whether LC19 differs molecularly and cellularly in patients with severe vs. mild acute disease was not addressed in this project due to the focus on a very well-described cohort of patients with a mild course of acute disease. Using single cell genomics, we were able to identify cell type-specific differences between LC19 patients and recovered patients after acute COVID disease, especially in monocytes, NK cells and T cells. Our results now offer the opportunity to verify the molecular signatures in further studies for the diagnosis of LC-19, to follow them in clinical studies and to correlate them with therapy outcome.

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