SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis

A study published in Cell using transcriptomic, radiological and histopathological data showed that SARS-CoV-2 infection induced an influx of profibrotic macrophages (CD163) into the lung. The phenotype of CD163-macropages was similar to that seen during the development of idiopathic pulmonary fibrosis. Interestingly, exposure of human monocytes (macrophage precursors) to SARS-CoV-2, but not to influenza A or other viral RNA analogs, was sufficient to induce a similar profibrotic phenotype in vitro, which explains the cellular mechanism of pulmonary fibrosis in COVID-19 patients.