Abstract
SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) is the coronavirus strain causing the respiratory pandemic COVID-19 (coronavirus disease 2019). To understand the pathobiology of SARS-CoV-2 in humans it is necessary to unravel the metabolic changes that are produced in the individuals once the infection has taken place. The goal of this work is to provide new information about the altered biomolecule profile and with that the altered biological pathways of patients in different clinical situations due to SARS-CoV-2 infection. This is done via metabolomics using HPLC–QTOF–MS analysis of plasma samples at COVID-diagnose from a total of 145 adult patients, divided into different clinical stages based on their subsequent clinical outcome (25 negative controls (non-COVID); 28 positive patients with asymptomatic disease not requiring hospitalization; 27 positive patients with mild disease defined by a total time in hospital lower than 10 days; 36 positive patients with severe disease defined by a total time in hospital over 20 days and/or admission at the ICU; and 29 positive patients with fatal outcome or deceased). Moreover, follow up samples between 2 and 3 months after hospital discharge were also obtained from the hospitalized patients with mild prognosis. The final goal of this work is to provide biomarkers that can help to better understand how the COVID-19 illness evolves and to predict how a patient could progress based on the metabolites profile of plasma obtained at an early stage of the infection. In the present work, several metabolites were found as potential biomarkers to distinguish between the end-stage and the early-stage (or non-COVID) disease groups. These metabolites are mainly involved in the metabolism of carnitines, ketone bodies, fatty acids, lysophosphatidylcholines/phosphatidylcholines, tryptophan, bile acids and purines, but also omeprazole. In addition, the levels of several of these metabolites decreased to “normal” values at hospital discharge, suggesting some of them as early prognosis biomarkers in COVID-19 at diagnose.
Highlights
SARS-CoV-2 is the coronavirus strain causing the respiratory pandemic COVID-19
There are still many difficulties for an accurate SARS-CoV-2 patient’s risk categorization, which are consequences of COVID-19 complexity since coronavirus infection reflects a broad spectrum of patient symptoms, and as a result, diverse pathophysiological pathways are perturbed during the disease course
To yield a wider view of the metabolomics changes during the course of disease in COVID-19 patients, an untargeted metabolomics analysis based on RP/HPLC-qTOF mass spectrometry (MS)/MS analysis using two different ionization modes (ESI (+) and ESI (−)) was applied to increase the coverage of identified metabolites
Summary
SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) is the coronavirus strain causing the respiratory pandemic COVID-19 (coronavirus disease 2019). There are still many difficulties for an accurate SARS-CoV-2 patient’s risk categorization, which are consequences of COVID-19 complexity since coronavirus infection reflects a broad spectrum of patient symptoms, and as a result, diverse pathophysiological pathways are perturbed during the disease course This complexity has taken to many groups to investigate this exciting topic using metabolomics, given that the circulating metabolome provides a snapshot of the physiological state of the organism[1,2]. Metabolomics has shown that it is possible to differentiate plasma metabolite profiles of COVID-19 survivors with abnormal pulmonary function from those of healthy donors or subjects with normal pulmonary function These alterations mainly involved amino acid and glycerophospholipid metabolic pathways, increased levels of triacylglycerols (TG), phosphatidylcholines (PC), prostaglandin E2, arginine, and decreased levels of betain and a denosine[6]. The level of guanosine monophosphate was found to be modulated along with carbamoyl phosphate in mild to severe patients, suggesting the role of immune dysfunction and nucleotide metabolism in the progression of non/severe COVID-19 to severe c ondition[9]
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