As EBNA-1-specific memory CD4 T cells [198] may cross-react with citrulline in individuals with SE-positive HLA-DRB1 risk alleles, EBV infection coupled with this host’s HLA-DRB1 genetic predisposition may contribute to the pathophysiology of RA by reducing the immune system’s ability to control EBV-transformed cells, causing an increased exposure to EBV antigens, and chronic inflammation [189]. Here, HLA-DRB1 is linked to Epstein-Barr virus infection.