LAUSR

ABSTRACT Hepatitis B virus (HBV) is increasingly recognized for its involvement in extrahepatic diseases, including rheumatological manifestations such as arthritis and joint pain. This review introduces the concept of the liver-joint axis, hypothesizing that HBV may contribute to rheumatoid arthritis (RA) pathogenesis through immune and metabolic dysregulation. We emphasize the effect of HBV infection on fibroblast activation, metabolic reprogramming, and Th17/Treg imbalance. Transcriptome analysis further elucidates the complex signaling networks underlying HBV-associated RA. These findings support a pathogenic role for HBV in joint inflammation and suggest novel therapeutic opportunities for targeting HBV-driven RA.