The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that emerged in late 2019 has spread globally, causing a pandemic of respiratory illness designated coronavirus disease 2019 (COVID-19). Little is known about the host tissue and cellular responses associated with infection, symptoms and disease severity. As the consequences of the illness unfolds, it is clear that survival is accompanied by complex and damaging respiratory sequelae due to hyperactivated inflammatory immune cells linked to destructive lung damage, even in mild cases. A better definition of the pulmonary host response to SARS-CoV-2 infection is required to understand viral pathogenesis and to validate putative COVID-19 biomarkers that have been proposed in clinical studies. Here, we’ve used innovative, cutting-edge spatial transcriptomics approaches to delineate tissue signatures unique to COVID-19 and common across acute respiratory distress syndrome.
1. Describe the differences seen in gene expression between COVID-19 and ARDS lung tissue.
2. Explain how hyperactivated inflammatory immune cells can lead to lung damage in COVID-19.
3. Discuss how spatial transcriptomics can be used to study gene expression in FFPE tissue sections from COVID-19 autopsies.