Systems level insights into the impact of airborne exposure on SARS-CoV-2 pathogenesis and COVID-19 outcome - A multi-omics big data study

Jeganathan Manivannan; Lakshmikirupa Sundaresan

doi:10.1016/j.genrep.2021.101312

Systems level insights into the impact of airborne exposure on SARS-CoV-2 pathogenesis and COVID-19 outcome - A multi-omics big data study

Gene Rep. 2021 Dec:25:101312. doi: 10.1016/j.genrep.2021.101312. Epub 2021 Aug 12.

Authors

Jeganathan Manivannan¹, Lakshmikirupa Sundaresan²

Affiliations

¹ Environmental Health and Toxicology Lab, Department of Environmental Sciences, School of Life Sciences, Bharathiar University, Coimbatore 641046, Tamil Nadu, India.
² Developmental & Stem Cell Biology Program, The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada.

Abstract

Coronavirus disease 2019 (COVID-19) is a viral pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that led to more than 800,00 deaths and continues to be a major threat worldwide. The scientific community has been studying the risk factors associated with SARS-CoV-2 infection and pathogenesis. Recent studies highlight the possible contribution of atmospheric air pollution, specifically particulate matter (PM) exposure as a co-factor in COVID-19 severity. Hence, meaningful translation of suitable omics datasets of SARS-CoV-2 infection and PM exposure is warranted to understand the possible involvement of airborne exposome on COVID-19 outcome. Publicly available transcriptomic data (microarray and RNA-Seq) related to COVID-19 lung biopsy, SARS-CoV-2 infection in epithelial cells and PM exposure (lung tissue, epithelial and endothelial cells) were obtained in addition with proteome and interactome datasets. System-wide pathway/network analysis was done through appropriate software tools and data resources. The primary findings are; 1. There is no robust difference in the expression of SARS-CoV-2 entry factors upon particulate exposure, 2. The upstream pathways associated with upregulated genes during SARS-CoV-2 infection considerably overlap with that of PM exposure, 3. Similar pathways were differentially expressed during SARS-CoV-2 infection and PM exposure, 4. SARS-CoV-2 interacting host factors were predicted to be associated with the molecular impact of PM exposure and 5. Differentially expressed pathways during PM exposure may increase COVID-19 severity. Based on the observed molecular mechanisms (direct and indirect effects) the current study suggests that airborne PM exposure has to be considered as an additional co-factor in the outcome of COVID-19.

Keywords: ACE2, angiotensin-converting enzyme 2; COVID-19; COVID19, coronavirus disease 2019; CTSB, cathepsin B; CTSL, cathepsin L; DEG, differentially expressed genes; GEO, Gene Expression Omnibus; GSEA, gene set enrichment analysis; IL-17, interleukin-17; Microarray; Omics; PM, particulate matter; PPAR, peroxisome proliferator-activated receptors; PPI, protein-protein interaction; PTM, post-translational modification; Particulate matter; Pathway analysis; Proteome; RNA-seq; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TLR, Toll-like receptor; TMPRSS2, transmembrane protease, serine 2; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor; X2K, eXpression2Kinases.