About: Evidence for structural protein damage and membrane lipid remodeling in red blood cells from COVID-19 patients

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About: Evidence for structural protein damage and membrane lipid remodeling in red blood cells from COVID-19 patients Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Evidence for structural protein damage and membrane lipid remodeling in red blood cells from COVID-19 patients
Creator	Alessandro, Angelo D'alessandro, Angelo Dzieciatkowska, Monika Francis, Richard Hansen, Kirk Hill, Ryan Hod, Eldad Hudson, Krystalyn Spitalnik, Steven Thomas, Tiffany Zimring, James Nemkov, Travis Stefanoni, Davide Buehler, Paul Issaian, Aaron
source	MedRxiv; Medline
abstract	The SARS-CoV-2 beta coronavirus is the etiological driver of COVID-19 disease, which is primarily characterized by shortness of breath, persistent dry cough, and fever. Because they transport oxygen, red blood cells (RBCs) may play a role in the severity of hypoxemia in COVID-19 patients. The present study combines state-of-the-art metabolomics, proteomics, and lipidomics approaches to investigate the impact of COVID-19 on RBCs from 23 healthy subjects and 29 molecularly-diagnosed COVID-19 patients. RBCs from COVID-19 patients had increased levels of glycolytic intermediates, accompanied by oxidation and fragmentation of ankyrin, spectrin beta, and the N-terminal cytosolic domain of band 3 (AE1). Significantly altered lipid metabolism was also observed, especially short and medium chain saturated fatty acids, acyl-carnitines, and sphingolipids. Nonetheless, there were no alterations of clinical hematological parameters, such as RBC count, hematocrit, and mean corpuscular hemoglobin concentration, with only minor increases in mean corpuscular volume. Taken together, these results suggest a significant impact of SARS-CoV-2 infection on RBC structural membrane homeostasis at the protein and lipid levels. Increases in RBC glycolytic metabolites are consistent with a theoretically improved capacity of hemoglobin to off-load oxygen as a function of allosteric modulation by high-energy phosphate compounds, perhaps to counteract COVID-19-induced hypoxia. Conversely, because the N-terminus of AE1 stabilizes deoxyhemoglobin and finely tunes oxygen off-loading, RBCs from COVID-19 patients may be incapable of responding to environmental variations in hemoglobin oxygen saturation when traveling from the lungs to peripheral capillaries and, as such, may have a compromised capacity to transport and deliver oxygen.
has issue date	2020-06-30(xsd:dateTime)
bibo:doi	10.1101/2020.06.29.20142703
bibo:pmid	32637980
has license	medrxiv
sha1sum (hex)	85f5b020c92807504ac5b03550f031c201459497
schema:url	https://doi.org/10.1101/2020.06.29.20142703
resource representing a document's title	Evidence for structural protein damage and membrane lipid remodeling in red blood cells from COVID-19 patients
has PubMed identifier	32637980
schema:publication	medRxiv : the preprint server for health sciences
resource representing a document's body	covid:85f5b020c92807504ac5b03550f031c201459497#body_text
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