Post-COVID-19 immune dysregulation and autoimmune sequelae.

Area of Science:

• Immunology
• Virology
• Autoimmunity

Background:

• SARS-CoV-2 infection causes significant immune dysregulation, including hyperinflammation and lymphopenia.
• Persistent immune responses post-viral clearance can lead to loss of self-tolerance and autoimmune conditions.

Purpose of the Study:

• To review mechanistic and clinical evidence linking SARS-CoV-2 infection to autoimmunity.
• To elucidate the pathways and factors contributing to post-COVID-19 autoimmune sequelae.

Main Methods:

• Critical review of mechanistic and clinical evidence.
• Analysis of viral entry mechanisms, immune pathways, and microbiome/metabolic alterations.
• Examination of clinical manifestations and autoantibody emergence.

Main Results:

• SARS-CoV-2 infection can trigger autoimmunity through molecular mimicry, bystander activation, and epitope spreading.
• Oral-gut microbiome dysbiosis and metabolic perturbations contribute to chronic inflammation and impaired tolerance.
• Clinical evidence shows neurological, hematological, endocrine, and systemic autoimmune syndromes post-infection.

Conclusions:

• SARS-CoV-2 can act as an amplifier of autoimmune reactions in genetically predisposed individuals.
• Understanding these mechanisms is crucial for developing preventive and therapeutic strategies for post-COVID-19 autoimmunity.