Elsevier

Gene Reports

Volume 25, December 2021, 101312
Gene Reports

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

https://doi.org/10.1016/j.genrep.2021.101312Get rights and content

Highlights

  • Air pollution has been proposed as a cofactor in determining the severity of COVID-19.

  • Considerable overlapping of upstream pathways associated with upregulated genes during SARS-CoV-2 infection with that of PM exposure

  • Differentially expressed pathways during PM exposure may increase COVID-19 severity.

  • PM exposure has direct effects on COVID-19 infections as evident by overlapping molecular mechanisms.

  • PM exposure may pose indirect effects in pathophysiology of COVID-19 by affecting the pulmonary and vascular system.

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.

Abbreviations

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

Keywords

COVID-19
Particulate matter
Omics
Microarray
RNA-seq
Proteome
Pathway analysis

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