Affiliations 

  • 1 Australian National Phenome Centre, Computational and Systems Medicine, Health Futures Institute, Murdoch University, Harry Perkins Building, Perth, WA 6150, Australia
  • 2 Bruker Pty Ltd., Preston, VIC 3072, Australia
  • 3 Centre for Molecular Medicine & Innovative Therapeutics, Murdoch University, Perth, WA 6150, Australia
  • 4 State Adult Burn Unit, Fiona Stanley Hospital, Murdoch, WA 6150, Australia
  • 5 Department of Microbiology, PathWest Laboratory Medicine, Perth, WA 6009, Australia
  • 6 Singapore National Neuro Science Centre, Singapore Mandalay Road, Singapore 308232, Singapore
  • 7 Medical School, Faculty of Health and Medical Sciences, University of Western Australia, Nedlands, WA 6009, Australia
J Proteome Res, 2021 May 07;20(5):2796-2811.
PMID: 33724837 DOI: 10.1021/acs.jproteome.1c00052

Abstract

We performed quantitative metabolic phenotyping of blood plasma in parallel with cytokine/chemokine analysis from participants who were either SARS-CoV-2 (+) (n = 10) or SARS-CoV-2 (-) (n = 49). SARS-CoV-2 positivity was associated with a unique metabolic phenotype and demonstrated a complex systemic response to infection, including severe perturbations in amino acid and kynurenine metabolic pathways. Nine metabolites were elevated in plasma and strongly associated with infection (quinolinic acid, glutamic acid, nicotinic acid, aspartic acid, neopterin, kynurenine, phenylalanine, 3-hydroxykynurenine, and taurine; p < 0.05), while four metabolites were lower in infection (tryptophan, histidine, indole-3-acetic acid, and citrulline; p < 0.05). This signature supports a systemic metabolic phenoconversion following infection, indicating possible neurotoxicity and neurological disruption (elevations of 3-hydroxykynurenine and quinolinic acid) and liver dysfunction (reduction in Fischer's ratio and elevation of taurine). Finally, we report correlations between the key metabolite changes observed in the disease with concentrations of proinflammatory cytokines and chemokines showing strong immunometabolic disorder in response to SARS-CoV-2 infection.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.