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Publications

Journal Article Research Support, Non-U.S. Gov't Epublish 5 citations

PubMed: 38235145 DOI: 10.3389/fimmu.2023.1335352

T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID.

Front Immunol 14:1335352

Authors: 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, Pierre Corbeau

Affiliations

  • Immunology Department, Nîmes University Hospital, Nîmes, France.
  • Institute of Human Genetics, UMR9002, Centre National de la Recherche Scientifique (CNRS) and Montpellier University, Montpellier, France.
  • Institut National de la Santé et de la Recherche Médicale (INSERM) U1124, Université de Paris, Paris, France.
  • Immunology Department, Montpellier University Hospital, Montpellier, France.
  • Surgical Intensive Care Department, Nîmes University Hospital, Nîmes, France.
  • Medical and Surgical Emergency Department, Nîmes University Hospital, Nîmes, France.
  • Gerontology Department, Nîmes University Hospital, Nîmes, France.
  • Infectious Diseases Department, Nîmes University Hospital, Nîmes, France.
  • Pediatrics Department, Nîmes University Hospital, Nîmes, France.
  • Laval University Research Center, Quebec City, QC, Canada.

Abstract

Background

As about 10% of patients with COVID-19 present sequelae, it is important to better understand the physiopathology of so-called long COVID.

Method

To 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.

Results

None 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).

Conclusions

Our 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.

MeSH

Cytokines, Infections, Immune System Diseases, Apoptosis, Cells, Cell Death, Cd4-Positive T-Lymphocytes, Sars Virus, Sars-Cov-2, Post-Acute Covid-19 Syndrome

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