Abstract
COVID-19 (Coronavirus Disease 2019) has been an ongoing pandemic, resulting in an increase in people being infected globally. Understanding the potential risk of infection for people under different respiratory system conditions is important and will help prevent disease spreading. We explored and collected five published and one unpublished single-cell respiratory system tissue transcriptome datasets, including idiopathic pulmonary fibrosis (IPF), aging lungs (mouse origin data), lung cancers, and smoked branchial epithelium, for specifically reanalyzing the ACE2 and TMPRSS2 expression profiles. Compared to normal people, we found that smoking and lung cancer increase the risk for COVID-19 infection due to a higher expression of ACE2 and TMPRSS2 in lung cells. Aged lung does not show increased risk for infection. IPF patients may have a lower risk for original COVID-19 infection due to lower expression in AT2 cells but may have a higher risk for severity due to a broader expression spectrum of TMPRSS2. Further investigation and validation on these cell types are required. Nonetheless, this is the first report to predict the risk and potential severity for COVID-19 infection for people with different respiratory system conditions. Our analysis is the first systematic description and analysis to illustrate how the underlying respiratory system conditions contribute to a higher infection risk.
Highlights
COVID-19 (Coronavirus Disease 2019), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been recognized as a global public health crisis, infecting more than more than 1 million people and causing more than 50,000 deaths (Early April, World Health Organization (WHO) statistic)
We explored five publicly available singlecell respiratory system tissue transcriptome datasets (GSE122960, GSE124872, GSE127465, GSE131391, and Adams dataset which is only available for interactive viewing) that focused on different conditions, including idiopathic pulmonary fibrosis (IPF), aging lungs, lung cancers, and smoked branchial epithelium, for reanalyzing the angiotensin-converting enzyme 2 (ACE2) and TMPRSS2 expression profiles (Adams et al, 2019; Angelidis et al, 2019; Duclos et al, 2019; Reyfman et al, 2019; Zilionis et al, 2019)
Compared to the normal lungs, we found the following: (1) IPF patients may have a lower risk for COVID-19 infection due to a lower expression in AT2 cells but may have a higher risk for severity due to a broader expression spectrum of TMPRSS2; (2) The infection risk for smoking people is slightly higher than for non-smokers due to a higher expression of TMPRSS2; (3) Reanalyzing mouse lung tissue data shows that aged lung does not have a higher risk for infection due to the non-significant change of ACE2 and TMPRSS2 expression; (4) Lung cancer could potentially produce novel cell types with a high TMPRSS2 expression, which might increase the risk of COVID-19 infection
Summary
COVID-19 (Coronavirus Disease 2019), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been recognized as a global public health crisis, infecting more than more than 1 million people and causing more than 50,000 deaths (Early April, WHO statistic). With the number of infections, death, and infected countries climbing even higher, the World Health Organization (WHO) has already declared the rapidly COVID-19 outbreak a pandemic. Estimated mortality following COVID-19 infection is considered a rate of 5.7% (5.5–5.9) (Baud et al, 2020). There exists a supporting treatment guideline, still no specific medicine is proved to effectively prevent or treat COVID-19, according to WHO. Understanding which population is under higher risk is a crucial task to prevent disease spreading and decrease the mortality
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