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Could metabolomics drive the fate of COVID-19 pandemic? A narrative review on lights and shadows.

Michele Mussap, +1 more
- 30 Jul 2021 - 
- Vol. 59, Iss: 12, pp 1891-1905
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TLDR
In this paper, a limited number of metabolomics-and lipidomics-based clinical studies in COVID-19 patients have been published and are discussed in this review, where remarkable alterations in the lipid and amino acid metabolism depict the molecular phenotype of subjects infected by SARS-CoV-2.
Abstract
Human Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) infection activates a complex interaction host/virus, leading to the reprogramming of the host metabolism aimed at the energy supply for viral replication. Alterations of the host metabolic homeostasis strongly influence the immune response to SARS-CoV-2, forming the basis of a wide range of outcomes, from the asymptomatic infection to the onset of COVID-19 and up to life-threatening acute respiratory distress syndrome, vascular dysfunction, multiple organ failure, and death. Deciphering the molecular mechanisms associated with the individual susceptibility to SARS-CoV-2 infection calls for a system biology approach; this strategy can address multiple goals, including which patients will respond effectively to the therapeutic treatment. The power of metabolomics lies in the ability to recognize endogenous and exogenous metabolites within a biological sample, measuring their concentration, and identifying perturbations of biochemical pathways associated with qualitative and quantitative metabolic changes. Over the last year, a limited number of metabolomics- and lipidomics-based clinical studies in COVID-19 patients have been published and are discussed in this review. Remarkable alterations in the lipid and amino acid metabolism depict the molecular phenotype of subjects infected by SARS-CoV-2; notably, structural and functional data on the lipids-virus interaction may open new perspectives on targeted therapeutic interventions. Several limitations affect most metabolomics-based studies, slowing the routine application of metabolomics. However, moving metabolomics from bench to bedside cannot imply the mere determination of a given metabolite panel; rather, slotting metabolomics into clinical practice requires the conversion of metabolic patient-specific data into actionable clinical applications.

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Citations
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Journal ArticleDOI

Machine learning and semi-targeted lipidomics identify distinct serum lipid signatures in hospitalized COVID-19-positive and COVID-19-negative patients

TL;DR: In this paper , a semi-targeted lipidomics analysis was performed using liquid chromatography coupled to mass spectrometry, and two hundred and eighty-three lipid species were identified and quantified.
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Profiling metabolites and lipoproteins in COMETA, an Italian cohort of COVID-19 patients

TL;DR: A Random Forest model built using the EDTA-plasma spectra of COVID-19 patients ≤21 days and Post CO VID-19 subjects, provided a high discrimination accuracy, indicating both the presence of a strong of the acute infection and the substantial metabolic healing of Post COVID -19 subjects.
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Link between serum lipid signature and prognostic factors in COVID-19 patients.

TL;DR: In this paper, the translation of lipidome signatures to link the effects of five critical clinical prognostic factors with the patients' outcomes was proposed, which appeared as candidate biomarkers to monitor disease progression and severity.
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Inflammatory Bowel Disease and COVID-19: How Microbiomics and Metabolomics Depict Two Sides of the Same Coin

TL;DR: The impact of gut dysbiosis, inflammation, oxidative stress, and increased energy demand on metabolic pathways involving key metabolites, such as tryptophan, phenylalanine, histidine, glutamine, succinate, citrate, and lipids are presented.
Journal ArticleDOI

Plasma Oxylipins and Their Precursors Are Strongly Associated with COVID-19 Severity and with Immune Response Markers

TL;DR: The results suggest that the altered oxylipin metabolism disrupts the expected shift from innate immune response to resolution of inflammation.
References
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