Respiratory viruses and systemic lupus erythematosus: Biomarkers and mechanisms leading to autoimmunity

Autoimmunity has been explored in various viral infections, and its relevance to respiratory viruses deserves more attention, especially its immune derangement during these infections, which could potentially trigger relapse and induction of many new cases. Our study aimed to utilize publicly available transcriptomic respiratory viral datasets of rhinovirus, influenza virus, respiratory syncytial virus, and COVID-19 to understand their autoimmune activation. Antibodies produced against the autoantigens associated with respiratory viruses resulted in the identification of three biomarker genes: TRIM21, ELANE, and CTSG. These genes are reported to be involved in the pathways of neuroactive ligand-receptor interaction, neutrophil extracellular trap formation, apoptosis, amebiasis, renin-angiotensin system, and lysosome, commonly triggering the systemic lupus erythematosus (SLE) pathway in genetically susceptible SLE patients. These results emphasize that the key genes are enriched mainly in the immune system process linking SLE pathogenesis. Literature sources suggest that the biomarkers induce autoreactivity through bystander activation and molecular mimicry which results in aberrant B-cell activation and the formation of neutrophil extracellular traps leading to autoimmunity. Thus, these key biomarkers indicate a new direction for early diagnosis, risk assessment, and treatment of respiratory virus infections and SLE pathogenesis.