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Inflammation-, immunothrombosis,- and autoimmune-feedback loops may lead to persistent neutrophil self-stimulation in

Alain R Thierry1,2, Dominique Salmon3

  • 1IRCM, Institute of Research on Cancerology of Montpellier, INSERM U1194, University of Montpellier, Montpellier, France.

Journal of Medical Virology
|August 27, 2024
PubMed

Insights

Neutrophils and neutrophil extracellular traps (NETs) may drive long COVID by creating self-sustaining loops of inflammation, immunothrombosis, and autoimmunity following SARS-CoV-2 infection.

Area of Science:

  • Immunology
  • Pathophysiology
  • Virology

Background:

  • Long COVID pathophysiology remains a significant challenge in contemporary medicine.
  • The direct link between SARS-CoV-2 infection and post-acute sequelae is not fully understood.
  • Neutrophils and neutrophil extracellular traps (NETs) are implicated in various inflammatory conditions.

Purpose of the Study:

  • To investigate the role of neutrophils and NETs in the pathophysiology of long COVID.
  • To hypothesize a mechanism involving positive feedback loops initiated by SARS-CoV-2 infection.
  • To explore the interconnection of inflammation, immunothrombosis, and autoimmunity in long COVID.

Main Methods:

  • The study proposes a hypothetical model based on current molecular, cellular, and physiological observations.
  • It considers the direct interaction between SARS-CoV-2 and neutrophils.
  • It examines the potential for sustained NETs production beyond the acute infection phase.

Main Results:

  • Hypothesizes that SARS-CoV-2 infection triggers positive feedback loops involving neutrophils and NETs.
  • Suggests that direct SARS-CoV-2 binding to neutrophils leads to exaggerated and prolonged NETs production.
  • Proposes that this sustained NETs release drives systemic inflammation, immunothrombosis, and autoimmunity.

Conclusions:

  • Neutrophil and NETs dysregulation is hypothesized as a central mechanism in long COVID.
  • This mechanism involves interconnected loops of inflammation, immunothrombosis, and autoimmunity.
  • Persistent NETs production may underlie ongoing organ damage and vascular complications observed in long COVID.

Keywords:
NETosisautoimmunityinflammationlong COVIDneutrophil extracellular trapsplateletsthrombosisviral persistence

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