Altered mitochondrial respiration in peripheral blood mononuclear cells of post-acute sequelae of SARS-CoV-2 infection

Sahera Dirajlal-Fargo, David P. Maison, Jared C. Durieux, Anastasia Andrukhiv, Nicholas Funderburg, Kate Ailstock, Mariana Gerschenson*, Grace A. Mccomsey

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Peripheral blood mononuclear cells (PBMC) mitochondrial respiration was measured ex vivo from participants without a history of COVID (n = 19), with a history of COVID and full recovery (n = 20), and with PASC (n = 20). Mean mitochondrial basal respiration, ATP-linked respiration, maximal respiration, spare respiration capacity, ATP-linked respiration, and non-mitochondrial respiration were highest in COVID + PASC+ (p ≤ 0.04). Every unit increase in non-mitochondrial respiration, ATP-linked respiration, basal respiration, spare respiration capacity, and maximal respiration increased the predicted odds of PASC between 1 % and 6 %. Mitochondrial dysfunction in PBMCs may be contributing to the etiology of PASC.

Original languageEnglish (US)
Article number101849
JournalMitochondrion
Volume75
DOIs
StatePublished - Mar 2024

Funding

This publication was made possible through the funding support of the Clinical and Translational Science Collaborative of Cleveland , # UL1TR002548 (to GAM) from the National Center for Advancing Translational Sciences (NCATS) component of the National Institutes of Health (NIH) and NIH roadmap for Medical Research. MG was supported by NIH grants # P20GM113134 and U54MD007601 . The contents of this article are solely the responsibility of the authors and do not necessarily represent the official views of UHCRC or the NIH. This publication was made possible through the funding support of the Clinical and Translational Science Collaborative of Cleveland, #UL1TR002548 (to GAM) from the National Center for Advancing Translational Sciences (NCATS) component of the National Institutes of Health (NIH) and NIH roadmap for Medical Research. MG was supported by NIH grants #P20GM113134 and U54MD007601. The contents of this article are solely the responsibility of the authors and do not necessarily represent the official views of UHCRC or the NIH. We thank the study participants. This publication was made possible through funding support of the Clinical and Translational Science Collaborative of Cleveland which is funded by the National Institutes of Health, National Center for Advancing Translational Sciences, Clinical and Translational Science Award grant, UL1TR002548; and through support from the John A. Burns School of Medicine (JABSOM) at the University of Hawaii. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of NIH or JABSOM. Fig. 1 , Fig. 2 , Fig. 4 , and Fig. 5 created with BioRender.com. Fig. 3 compiled with BioRender.com. Fig. 2 and Fig. 4 adapted “Electron Transport Chain” by BioRender.com (2023). Fig. 1 adapted from “Expression of ACE2 Receptor in Human Host Tissues” by BioRender.com (2023). Retrieved from https://app.biorender.com/biorender-templates.

Keywords

  • COVID
  • Long COVID
  • Mitochondria
  • PASC

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Cell Biology

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