tetano
Editor, Senior Moderator
Nat Commun
. 2021 Jan 4;12(1):4.
doi: 10.1038/s41467-020-20323-9.
The aging transcriptome and cellular landscape of the human lung in relation to SARS-CoV-2
Ryan D Chow[SUP] 1 2 3 4 [/SUP], Medha Majety[SUP] 1 2 3 5 [/SUP], Sidi Chen[SUP] 6 7 8 9 10 11 12 13 14 15 16 17 18 [/SUP]
Affiliations
Abstract
Age is a major risk factor for severe coronavirus disease-2019 (COVID-19). Here, we interrogate the transcriptional features and cellular landscape of the aging human lung. By intersecting these age-associated changes with experimental data on SARS-CoV-2, we identify several factors that may contribute to the heightened severity of COVID-19 in older populations. The aging lung is transcriptionally characterized by increased cell adhesion and stress responses, with reduced mitochondria and cellular replication. Deconvolution analysis reveals that the proportions of alveolar type 2 cells, proliferating basal cells, goblet cells, and proliferating natural killer/T cells decrease with age, whereas alveolar fibroblasts, pericytes, airway smooth muscle cells, endothelial cells and IGSF21[SUP]+[/SUP] dendritic cells increase with age. Several age-associated genes directly interact with the SARS-CoV-2 proteome. Age-associated genes are also dysregulated by SARS-CoV-2 infection in vitro and in patients with severe COVID-19. These analyses illuminate avenues for further studies on the relationship between age and COVID-19.
. 2021 Jan 4;12(1):4.
doi: 10.1038/s41467-020-20323-9.
The aging transcriptome and cellular landscape of the human lung in relation to SARS-CoV-2
Ryan D Chow[SUP] 1 2 3 4 [/SUP], Medha Majety[SUP] 1 2 3 5 [/SUP], Sidi Chen[SUP] 6 7 8 9 10 11 12 13 14 15 16 17 18 [/SUP]
Affiliations
- PMID: 33397975
- DOI: 10.1038/s41467-020-20323-9
Abstract
Age is a major risk factor for severe coronavirus disease-2019 (COVID-19). Here, we interrogate the transcriptional features and cellular landscape of the aging human lung. By intersecting these age-associated changes with experimental data on SARS-CoV-2, we identify several factors that may contribute to the heightened severity of COVID-19 in older populations. The aging lung is transcriptionally characterized by increased cell adhesion and stress responses, with reduced mitochondria and cellular replication. Deconvolution analysis reveals that the proportions of alveolar type 2 cells, proliferating basal cells, goblet cells, and proliferating natural killer/T cells decrease with age, whereas alveolar fibroblasts, pericytes, airway smooth muscle cells, endothelial cells and IGSF21[SUP]+[/SUP] dendritic cells increase with age. Several age-associated genes directly interact with the SARS-CoV-2 proteome. Age-associated genes are also dysregulated by SARS-CoV-2 infection in vitro and in patients with severe COVID-19. These analyses illuminate avenues for further studies on the relationship between age and COVID-19.