Multiomics integration-based molecular characterizations of COVID-19

Abstract

The coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), rapidly became a global health challenge, leading to unprecedented social and economic consequences. The mechanisms behind the pathogenesis of SARS-CoV-2 are both unique and complex. Omics-scale studies are emerging rapidly and offer a tremendous potential to unravel the puzzle of SARS-CoV-2 pathobiology, as well as moving forward with diagnostics, potential drug targets, risk stratification, therapeutic responses, vaccine development and therapeutic innovation. This review summarizes various aspects of understanding multiomics integration-based molecular characterizations of COVID-19, which to date include the integration of transcriptomics, proteomics, genomics, lipidomics, immunomics and metabolomics to explore virus targets and developing suitable therapeutic solutions through systems biology tools. Furthermore, this review also covers an abridgment of omics investigations related to disease pathogenesis and virulence, the role of host genetic variation and a broad array of immune and inflammatory phenotypes contributing to understanding COVID-19 traits. Insights into this review, which combines existing strategies and multiomics integration profiling, may help further advance our knowledge of COVID-19.

Glutathione deficiency in the pathogenesis of SARS-CoV-2 infection and its effects upon the host immune response in severe COVID-19 disease

“…The enhancement of Nrf2 transcription with sulforaphane or melatonin could benefit patients with “LONG COVID” (Post-Acute Sequelae of SARS-CoV-2 or Post-COVID-Syndrome), a significant proportion (approximately 40%) of individuals with COVID-19 experiencing a variety of symptoms (loss of smell and/or taste, fatigue, cough, aching pain, “brain fog,” insomnia, shortness of breath, and tachycardia) after 12 weeks ( Jarrott et al, 2022 ; Ordonez et al, 2022 ). Multi-omics studies revealed that SARS-CoV-2 infection provokes significant changes in numerous metabolites including those impacting on virus propagation (one-carbon metabolism) and GSH synthesis (amino acids glutamic acid, cysteine and glycine) that could be used as early prognosis biomarkers in COVID-19 at diagnose to predict severe COVID-19 and “LONG COVID” ( Doğan et al, 2021 ; Li C.-X. et al, 2022 ; Perła-Kaján and Jakubowski, 2022 ; Valdés et al, 2022 ).…”

COVIDomics: The Proteomic and Metabolomic Signatures of COVID-19

“…Since viruses are able to modulate lipid synthesis and signaling into the host cell to produce lipids for their envelopes by creating a lipid micro-environment ideal for replication, the lipid dysregulation is suggested as a drug target to prevent coronavirus infection [ 28 ]. Furthermore, considering the high heterogeneity of the clinical manifestations of COVID-19, thus suggesting the involvement of diverse pathophysiological processes [ 29 ], multiomics approaches and data integration analyses may result as a winning choice, contributing to a better understanding of the molecular biology of SARS-CoV-2 at every level of complexity [ 30 ].…”

New Discovery of Myeloid-Derived Suppressor Cell’s Tale on Viral Infection and COVID-19

“…Additionally, severe COVID-19associated hyperinflammatory syndromes have been reported that they originate from a host innate immune response (37). Studies of transcriptome, proteomic, and epigenomics have revealed a wide range of functional impairments, including marked neutrophil hyperactivation symptoms in severe COVID-19 (38)(39)(40)(41). Collectively, COVID-19 caused by SARS-CoV-2 is associated with a failure of innate and adaptive immune system regulation due to changes in other immune cells associated with a decrease in adaptive T cells.…”