A single-cell transcriptome landscape of COVID-19 patients’ lungs

A single-cell transcriptome landscape of COVID-19 patients’ lungs because the lung is the primary organ attacked by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), respiratory failure is a leading cause of death from the coronavirus disease 2019 (COVID-19). However, our understanding of how SARS-CoV-2 infection causes lung disease is restricted at the cellular and molecular level. We combined histological, transcriptomic, and proteomic investigations to create multi-omics and single-nucleus transcriptomic atlases of the lungs of COVID-19 patients. In distinct lung and infiltrating immune cell types, our research exposes the molecular underpinnings of pathological hallmarks associated with SARS-CoV-2 infection. We establish parenchymal lung senescence as a molecular state of COVID-19 pathology, and present molecular fingerprints of hyperinflammation, alveolar epithelial cell exhaustion, vascular alterations, and fibrosis. Furthermore, our findings imply that FOXO3A suppression may be a factor in the fibroblast-to-myofibroblast transition seen in COVID-19 pulmonary fibrosis. Our research portrays a comprehensive cellular and molecular atlas of the lungs of COVID-19 patients and sheds light on SARS-CoV-2-related pulmonary injury, allowing biomarkers to be identified and symptomatic therapies to be developed.

Chapter I Surface Anatomy and Anterior Body Landmarks

COVID-19 pathology transcriptomic and proteomic analyses

We collected post-mortem lung tissue samples from COVID-19 patients with an average age of 66 years. As controls, we gathered age-matched normal lung samples from a group of people who had no known history of infectious illnesses. We discovered a spectrum of diffuse alveolar damage defined by desquamation of the alveolar epithelium and the formation of mucous plugs after histological investigation of SARS-CoV-2-infected lung parenchyma. With disseminated intravascular coagulation, we were able to detect vascular damage as well. In addition, there was a lot of intra-alveolar macrophage infiltration, a lot of lung fibrosis, and a lot of apoptosis.

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