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We developed a computational pipeline (Fig. 1b–d and data not shown) and was used for the remaining samples.
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Although initial tests showed some differences in proportions of cell types between snRNA-Seq and scRNA-Seq, snRNA-Seq performed better overall 13 (Extended Data Fig. Our atlases provide crucial insights into the pathogenesis of severe COVID-19. Here, we developed a large cross-body COVID-19 autopsy biobank of 420 autopsy specimens, spanning 11 organs, and used it to generate a single-cell atlas of lung, kidney, liver and heart associated with COVID-19 and a lung spatial atlas, in a subset of 14–18 donors per organ. Autopsies are crucial to understanding severe COVID-19 pathophysiology 9, 10, 11, 12, but comprehensive genomic studies are challenged by long post-mortem intervals (PMIs). Many molecular and cellular questions related to COVID-19 pathophysiology remain unanswered, including how cell composition and gene programs shift, which cells are infected, and how associated genetic loci drive disease. Severe COVID-19 is also accompanied by an inappropriate pro-inflammatory host immune response and a diminished antiviral interferon response 6, 7, 8. Clinical deterioration in acute illness leads to ineffective viral clearance and collateral tissue damage 1, 2, 3, 4, 5. The leading cause of mortality is acute lung injury and acute respiratory distress syndrome, or direct complications with multiple organ failure 1, 2, 3, 4. The host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection ranges from asymptomatic infection to severe coronavirus disease 2019 (COVID-19) and death. Our foundational dataset elucidates the biological effect of severe SARS-CoV-2 infection across the body, a key step towards new treatments. Analysis of the other tissue atlases showed transcriptional alterations in multiple cell types in heart tissue from donors with COVID-19, and mapped cell types and genes implicated with disease severity based on COVID-19 genome-wide association studies.
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Spatial analysis in lung distinguished inflammatory host responses in lung regions with and without viral RNA. Viral RNAs were enriched in mononuclear phagocytic and endothelial lung cells, which induced specific host programs. Integrated computational analysis uncovered substantial remodelling in the lung epithelial, immune and stromal compartments, with evidence of multiple paths of failed tissue regeneration, including defective alveolar type 2 differentiation and expansion of fibroblasts and putative TP63 + intrapulmonary basal-like progenitor cells. Here we generated single-cell atlases of 24 lung, 16 kidney, 16 liver and 19 heart autopsy tissue samples and spatial atlases of 14 lung samples from donors who died of COVID-19. Nature volume 595, pages 107–113 ( 2021) Cite this articleĬOVID-19, which is caused by SARS-CoV-2, can result in acute respiratory distress syndrome and multiple organ failure 1, 2, 3, 4, but little is known about its pathophysiology. COVID-19 tissue atlases reveal SARS-CoV-2 pathology and cellular targets