Abstract
Background. Recovery from coronavirus disease 2019 (COVID-19) probably leads to long-term symptoms, including immune system complications. Recent publications have reported that severe acute respiratory syndrome-associated coronavirus-2 (SARS-CoV-2) infection or, sometimes, vaccination against it may trigger autoimmune responses in vulnerable cohorts. Purpose of the research. To investigate the differences in the expression of the Protein tyrosine phosphatase non-receptor type 22 (PTPN22), Tumor necrosis factor receptor-associated factor 1 (TRAF-1) and Interleukin-1 beta (IL-1β) genes in patients with rheumatoid arthritis (RA) and healthy controls following SARS-CoV-2 infection or vaccination. Methods. Blood samples were collected from 61 patients diagnosed with RA post COVID-19 Rheumatoid arthritis patients after SARS-CoV-2 infection (RAI), and 40 controls (C) who had experienced at least one COVID-19 infection. RNA was extracted and used to prepare cDNA from each sample and was then used to analyse the expression of PTPN22, TRAF-1 and IL-1β using relative gene expression. Results. The study covered all 61 patients; 17 had been vaccinated without prior COVID-19 infection Rheumatoid arthritis patients after SARS-CoV-2 vaccination (RAV), while 44 were diagnosed with RA after recovery from COVID-19 (RAI). A statistically significant decrease in the gene expression of TRAF-1 was observed in both RAI and (RAV) patients compared with the C group (P=0.042). A consistently significant increase in gene expression of IL-1β was observed in both RAI and RAV samples compared with controls. However, the reduction in PTPN22 expression was not statistically significant. Conclusion. In this study, TRAF-1 was significantly downregulated, but IL-1β was upregulated in patients with RA post either COVID-19 infection or vaccination, while PTPN22 showed a non-significant reduction. The study findings suggest that triggered immune response post SARS-CoV-2 exposure, through infection or vaccination, may influence molecular pathways involved in RA pathogenesis.