# Liver–joint axis: Hepatitis B virus as a contributor to rheumatoid arthritis pathogenesis

## TL;DR

This paper explores how Hepatitis B virus might contribute to rheumatoid arthritis through immune and metabolic changes, introducing the liver-joint axis concept.

## Contribution

The paper introduces the novel concept of a liver-joint axis linking HBV to rheumatoid arthritis through immune and metabolic dysregulation.

## Key findings

- HBV infection affects fibroblast activation and metabolic reprogramming.
- HBV contributes to Th17/Treg imbalance, which may drive joint inflammation.
- Transcriptome analysis reveals signaling networks involved in HBV-associated rheumatoid arthritis.

## 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.