T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID
BackgroundAs about 10% of patients with COVID-19 present sequelae, it is important to better understand the physiopathology of so-called long COVID.MethodTo this aim, we recruited 29 patients hospitalized for SARS-CoV-2 infection and, by Luminex®, quantified 19 soluble factors in their plasma and in...
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Frontiers Media S.A.
2024-01-01
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Series: | Frontiers in Immunology |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2023.1335352/full |
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author | Renaud Cezar Lucy Kundura Sonia André Claire Lozano Thierry Vincent Laurent Muller Jean-Yves Lefrant Claire Roger Pierre-Géraud Claret Sandra Duvnjak Paul Loubet Albert Sotto Tu-Ahn Tran Jérôme Estaquier Jérôme Estaquier Pierre Corbeau Pierre Corbeau |
author_facet | Renaud Cezar Lucy Kundura Sonia André Claire Lozano Thierry Vincent Laurent Muller Jean-Yves Lefrant Claire Roger Pierre-Géraud Claret Sandra Duvnjak Paul Loubet Albert Sotto Tu-Ahn Tran Jérôme Estaquier Jérôme Estaquier Pierre Corbeau Pierre Corbeau |
author_sort | Renaud Cezar |
collection | DOAJ |
description | BackgroundAs about 10% of patients with COVID-19 present sequelae, it is important to better understand the physiopathology of so-called long COVID.MethodTo this aim, we recruited 29 patients hospitalized for SARS-CoV-2 infection and, by Luminex®, quantified 19 soluble factors in their plasma and in the supernatant of their peripheral blood mononuclear cells, including inflammatory and anti-inflammatory cytokines and chemokines, Th1/Th2/Th17 cytokines, and endothelium activation markers. We also measured their T4, T8 and NK differentiation, activation, exhaustion and senescence, T cell apoptosis, and monocyte subpopulations by flow cytometry. We compared these markers between participants who developed long COVID or not one year later.ResultsNone of these markers was predictive for sequelae, except programmed T4 cell death. T4 lymphocytes from participants who later presented long COVID were more apoptotic in culture than those of sequelae-free participants at Month 12 (36.9 ± 14.7 vs. 24.2 ± 9.0%, p = 0.016).ConclusionsOur observation raises the hypothesis that T4 cell death during the acute phase of SARS-CoV-2 infection might pave the way for long COVID. Mechanistically, T4 lymphopenia might favor phenomena that could cause sequelae, including SARS-CoV-2 persistence, reactivation of other viruses, autoimmunity and immune dysregulation. In this scenario, inhibiting T cell apoptosis, for instance, by caspase inhibitors, could prevent long COVID. |
first_indexed | 2024-03-08T17:22:11Z |
format | Article |
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institution | Directory Open Access Journal |
issn | 1664-3224 |
language | English |
last_indexed | 2024-03-08T17:22:11Z |
publishDate | 2024-01-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Immunology |
spelling | doaj.art-d8b84236ac6c4142884fcaf274d018e32024-01-03T04:43:16ZengFrontiers Media S.A.Frontiers in Immunology1664-32242024-01-011410.3389/fimmu.2023.13353521335352T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVIDRenaud Cezar0Lucy Kundura1Sonia André2Claire Lozano3Thierry Vincent4Laurent Muller5Jean-Yves Lefrant6Claire Roger7Pierre-Géraud Claret8Sandra Duvnjak9Paul Loubet10Albert Sotto11Tu-Ahn Tran12Jérôme Estaquier13Jérôme Estaquier14Pierre Corbeau15Pierre Corbeau16Immunology Department, Nîmes University Hospital, Nîmes, FranceInstitute of Human Genetics, UMR9002, Centre National de la Recherche Scientifique (CNRS) and Montpellier University, Montpellier, FranceInstitut National de la Santé et de la Recherche Médicale (INSERM) U1124, Université de Paris, Paris, FranceImmunology Department, Montpellier University Hospital, Montpellier, FranceImmunology Department, Montpellier University Hospital, Montpellier, FranceSurgical Intensive Care Department, Nîmes University Hospital, Nîmes, FranceSurgical Intensive Care Department, Nîmes University Hospital, Nîmes, FranceSurgical Intensive Care Department, Nîmes University Hospital, Nîmes, FranceMedical and Surgical Emergency Department, Nîmes University Hospital, Nîmes, FranceGerontology Department, Nîmes University Hospital, Nîmes, FranceInfectious Diseases Department, Nîmes University Hospital, Nîmes, FranceInfectious Diseases Department, Nîmes University Hospital, Nîmes, FrancePediatrics Department, Nîmes University Hospital, Nîmes, FranceInstitut National de la Santé et de la Recherche Médicale (INSERM) U1124, Université de Paris, Paris, France0Laval University Research Center, Quebec City, QC, CanadaImmunology Department, Nîmes University Hospital, Nîmes, FranceInstitute of Human Genetics, UMR9002, Centre National de la Recherche Scientifique (CNRS) and Montpellier University, Montpellier, FranceBackgroundAs about 10% of patients with COVID-19 present sequelae, it is important to better understand the physiopathology of so-called long COVID.MethodTo this aim, we recruited 29 patients hospitalized for SARS-CoV-2 infection and, by Luminex®, quantified 19 soluble factors in their plasma and in the supernatant of their peripheral blood mononuclear cells, including inflammatory and anti-inflammatory cytokines and chemokines, Th1/Th2/Th17 cytokines, and endothelium activation markers. We also measured their T4, T8 and NK differentiation, activation, exhaustion and senescence, T cell apoptosis, and monocyte subpopulations by flow cytometry. We compared these markers between participants who developed long COVID or not one year later.ResultsNone of these markers was predictive for sequelae, except programmed T4 cell death. T4 lymphocytes from participants who later presented long COVID were more apoptotic in culture than those of sequelae-free participants at Month 12 (36.9 ± 14.7 vs. 24.2 ± 9.0%, p = 0.016).ConclusionsOur observation raises the hypothesis that T4 cell death during the acute phase of SARS-CoV-2 infection might pave the way for long COVID. Mechanistically, T4 lymphopenia might favor phenomena that could cause sequelae, including SARS-CoV-2 persistence, reactivation of other viruses, autoimmunity and immune dysregulation. In this scenario, inhibiting T cell apoptosis, for instance, by caspase inhibitors, could prevent long COVID.https://www.frontiersin.org/articles/10.3389/fimmu.2023.1335352/fullprogrammed cell deathpost-acute COVID-19 syndromeimmune activationhelper T lymphocyteSARS-CoV-2 infection sequelae |
spellingShingle | Renaud Cezar Lucy Kundura Sonia André Claire Lozano Thierry Vincent Laurent Muller Jean-Yves Lefrant Claire Roger Pierre-Géraud Claret Sandra Duvnjak Paul Loubet Albert Sotto Tu-Ahn Tran Jérôme Estaquier Jérôme Estaquier Pierre Corbeau Pierre Corbeau T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID Frontiers in Immunology programmed cell death post-acute COVID-19 syndrome immune activation helper T lymphocyte SARS-CoV-2 infection sequelae |
title | T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID |
title_full | T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID |
title_fullStr | T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID |
title_full_unstemmed | T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID |
title_short | T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID |
title_sort | t4 apoptosis in the acute phase of sars cov 2 infection predicts long covid |
topic | programmed cell death post-acute COVID-19 syndrome immune activation helper T lymphocyte SARS-CoV-2 infection sequelae |
url | https://www.frontiersin.org/articles/10.3389/fimmu.2023.1335352/full |
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