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

Human Cell Atlas Lung, 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 KaminskiJonathan A. Kropski, Nicholas E. Banovich*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

30 Citations (Scopus)
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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. Patients with chronic lung disease (CLD) have an increased risk for severe coronavirus disease-19 and poor outcomes. Here the authors compare the transcriptomes of single cells isolated from healthy and CLD lungs to identify molecular characteristics of lung cells that may account for worse COVID-19 outcomes in these patients.

Original languageEnglish
Article number4314
Number of pages13
JournalNature Communications
Volume12
Issue number1
DOIs
Publication statusPublished - 14-Jul-2021

Keywords

  • RECEPTOR ACE2
  • COVID-19

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