Highly relevant article out in Nature describing l

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When spatially contextualizing these interactions, we observed that macrophages preferentially interact with fibroblasts in the alveolar walls, suggesting a contribution to fibrosis and thickening of the alveolar wall in late disease (Fig. 2h)

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However, pathways related with angiogenesis, myogenesis and epithelial-to-mesenchymal transition were increased in COVID-19 compared with healthy lungs and progressively with late disease (ED9b). In accordance with the IMC data, we also observed that coagulation, complement activation, and apoptosis pathways were upregulated in alveolar areas, but also in blood vessels in late COVID-19 (ED9c). This suggests that after an early disease period dominated by inflammatory responses to SARS-CoV-2, late COVID-19 in the lung may be driven by pathogen-independent mechanisms which are a consequence of an immune response with aberrant resolution.

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While our analysis agrees with recent reports that indicate the type of pathophysiological response to SARS-CoV-2 infection may not be entirely different from ARDS unrelated to COVID-19 , it is at odds with reports suggesting that the hyper-inflammatory phenotype as assessed by cytokine levels in peripheral blood is not COVID-19 specific . Our observation that Spike alveolar epithelial cells do not differentially interact with cells of the immune system despite extensive immune infiltration in the lung, potentially high- lights the lack of “on-target” immunological response, while the high amount of complement activation in COVID-19 lung tissue likely results in indiscriminate “off-target” tissue damage, exacerbating COVID-19 disease and continuing the cycle of inflammation

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