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Evidence of Structural Protein Damage and Membrane Lipid Remodeling in Red Blood Cells from COVID-19 Patients, 2020, Thomas et al

Discussion in 'Epidemics (including Covid-19)' started by Theo, Nov 20, 2020.

  1. Theo

    Theo Established Member (Voting Rights)

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    Both red blood cells damage and kynurine identified in LongCovid research

    https://news.cuanschutz.edu/news-st...1b-VxUN-n6F55E6dMVcMwGkMR-huuW-wbi8mEvqTNJt-s

     
    Last edited by a moderator: Nov 20, 2020
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  2. rvallee

    rvallee Senior Member (Voting Rights)

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  3. Hutan

    Hutan Moderator Staff Member

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    This is the red blood cell paper referred to in the article:

    Evidence of Structural Protein Damage and Membrane Lipid Remodeling in Red Blood Cells from COVID-19 Patients
    https://pubs.acs.org/doi/10.1021/acs.jproteome.0c00606

    Abstract

    [​IMG]

    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, in particular, 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, or 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 and metabolic rewiring toward the hexose monophosphate shunt, RBCs from COVID-19 patients may be less capable of responding to environmental variations in hemoglobin oxygen saturation/oxidant stress when traveling from the lungs to peripheral capillaries and vice versa.
     
    Last edited: Nov 20, 2020
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  4. Hutan

    Hutan Moderator Staff Member

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    The article is readable and interesting.

    It's not exactly clear that the researcher mentioned in the article has yet recovered, although he is attributing his ongoing effects first to damage to his red blood cells (which should be corrected when there are new red blood cells) and now inflammation in the lungs, rather than ME/CFS. He'd be a handy researcher to have working on ME/CFS.


    Kynurine is mentioned in relation to a forthcoming study:
     
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