Chandelier
Senior Member (Voting Rights)
Post-COVID-19 immune dysregulation and autoimmune sequelae
Abdel-Moneim, Ahmed S.; Al-Balushi, Mohammad S.; Al-Jabri, Ali A.
In some individuals, these responses persist beyond viral clearance, creating conditions that may disrupt immunological self-tolerance and precipitate autoimmune phenomena.
We critically review mechanistic and clinical evidence linking SARS-CoV-2 infection to autoimmunity.
Viral entry via ACE2/TMPRSS2, endothelial injury, and renin–angiotensin system dysregulation generates a pro-inflammatory milieu.
Immune pathways, including molecular mimicry, bystander activation, epitope spreading, and persistent antigenic stimulation, can trigger the activation of autoreactive lymphocytes.
Emerging evidence further implicates SARS-CoV-2-associated oral-gut microbiome dysbiosis and alterations in tryptophan and arginine metabolic checkpoints as contributors to chronic inflammatory signaling and impaired tolerance maintenance.
We propose a mechanistic cascade from viral infection to dysbiosis to metabolic perturbation to loss of tolerance to autoantibody generation.
Clinical manifestations encompass neurological, hematological, endocrine, and systemic autoimmune syndromes, with evidence of autoantibody emergence and post-COVID-19 immune sequelae.
SARS-CoV-2 acts as an amplifier of autoimmune reaction in genetically susceptible hosts.
Understanding these mechanisms is critical for identifying at-risk individuals and informing preventive and therapeutic strategies for post-COVID-19 autoimmune sequelae.
Web | DOI | Virology
Abdel-Moneim, Ahmed S.; Al-Balushi, Mohammad S.; Al-Jabri, Ali A.
Highlights
- SARS-CoV-2 infection can induce persistent immune dysregulation : hyperinflammation, lymphopenia, and innate–adaptive imbalance.
- Molecular mimicry, bystander activation, and epitope spreading, may link SARS-CoV-2 infection to autoimmunity.
- ACE2/TMPRSS2-mediated viral entry and endothelial injury may disrupt immune tolerance.
- Post-COVID autoimmune manifestations involve neurological, hematological, endocrine, and systemic disorders.
- SARS-CoV-2 may act as a trigger or amplifier of autoimmunity in genetically susceptible individuals.
Abstract
SARS-CoV-2 infection induces profound immune dysregulation, including hyperinflammation, lymphopenia, and innate/adaptive immune imbalance.In some individuals, these responses persist beyond viral clearance, creating conditions that may disrupt immunological self-tolerance and precipitate autoimmune phenomena.
We critically review mechanistic and clinical evidence linking SARS-CoV-2 infection to autoimmunity.
Viral entry via ACE2/TMPRSS2, endothelial injury, and renin–angiotensin system dysregulation generates a pro-inflammatory milieu.
Immune pathways, including molecular mimicry, bystander activation, epitope spreading, and persistent antigenic stimulation, can trigger the activation of autoreactive lymphocytes.
Emerging evidence further implicates SARS-CoV-2-associated oral-gut microbiome dysbiosis and alterations in tryptophan and arginine metabolic checkpoints as contributors to chronic inflammatory signaling and impaired tolerance maintenance.
We propose a mechanistic cascade from viral infection to dysbiosis to metabolic perturbation to loss of tolerance to autoantibody generation.
Clinical manifestations encompass neurological, hematological, endocrine, and systemic autoimmune syndromes, with evidence of autoantibody emergence and post-COVID-19 immune sequelae.
SARS-CoV-2 acts as an amplifier of autoimmune reaction in genetically susceptible hosts.
Understanding these mechanisms is critical for identifying at-risk individuals and informing preventive and therapeutic strategies for post-COVID-19 autoimmune sequelae.
Web | DOI | Virology