Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity

Linh T. Bui, Nichelle I. Winters, Mei-I Chung, Chitra Joseph, Austin J. Gutierrez, Arun C. Habermann, Taylor S. Adams, Jonas C. Schupp, Sergio Poli, Lance M. Peter, Chase J. Taylor, Jessica B. Blackburn, Bradley W. Richmond, Andrew G. Nicholson, Doris Rassl, William A. Wallace, Ivan O. Rosas, R. Gisli Jenkins, Naftali Kaminski, Jonathan A. Kropski and Nicholas E. Banovich ()
Additional contact information
Linh T. Bui: Translational Genomics Research Institute
Nichelle I. Winters: Vanderbilt University Medical Center
Mei-I Chung: Translational Genomics Research Institute
Chitra Joseph: University of Nottingham
Austin J. Gutierrez: Translational Genomics Research Institute
Arun C. Habermann: Vanderbilt University Medical Center
Taylor S. Adams: Yale School of Medicine
Jonas C. Schupp: Yale School of Medicine
Sergio Poli: Brigham and Women’s Hospital, Harvard Medical School
Lance M. Peter: Translational Genomics Research Institute
Chase J. Taylor: Vanderbilt University Medical Center
Jessica B. Blackburn: Vanderbilt University Medical Center
Bradley W. Richmond: Vanderbilt University Medical Center
Andrew G. Nicholson: Imperial College
Doris Rassl: Royal Papworth Hospital NHS Foundation Trust
William A. Wallace: Royal Infirmary of Edinburgh
Ivan O. Rosas: Baylor College of Medicine
R. Gisli Jenkins: University of Nottingham
Naftali Kaminski: Yale School of Medicine
Jonathan A. Kropski: Vanderbilt University Medical Center
Nicholas E. Banovich: Translational Genomics Research Institute

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: Abstract Patients with chronic lung disease (CLD) have an increased risk for severe coronavirus disease-19 (COVID-19) and poor outcomes. Here, we analyze the transcriptomes of 611,398 single cells isolated from healthy and CLD lungs to identify molecular characteristics of lung cells that may account for worse COVID-19 outcomes in patients with chronic lung diseases. We observe a similar cellular distribution and relative expression of SARS-CoV-2 entry factors in control and CLD lungs. CLD AT2 cells express higher levels of genes linked directly to the efficiency of viral replication and the innate immune response. Additionally, we identify basal differences in inflammatory gene expression programs that highlight how CLD alters the inflammatory microenvironment encountered upon viral exposure to the peripheral lung. Our study indicates that CLD is accompanied by changes in cell-type-specific gene expression programs that prime the lung epithelium for and influence the innate and adaptive immune responses to SARS-CoV-2 infection.

Date: 2021
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DOI: 10.1038/s41467-021-24467-0

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