Risk of hepatitis B virus reactivation in patients with autoimmune diseases undergoing non-tumor necrosis factor-targeted biologics

Abstract

Hepatitis B virus reactivation (HBVr) can occur in patients treated with immunosuppressive medications. Risk stratification for HBVr based on hepatitis B virus (HBV) serology and viral load is an important strategy to determine appropriate HBV monitoring and antiviral prophylaxis use. Recent advances in the understanding of pathophysiology of autoimmune diseases have led the development of cytokine-targeted therapies. Tumor necrosis factor (TNF)-α inhibitors have been widely used for patients with inflammatory bowel disease, psoriasis, and rheumatic diseases. Further, the clinical benefits of interleukin (IL)-12/23, IL-17, or Janus kinases inhibitors have been demonstrated in these patients. It is well known that TNF-α inhibitor use can lead to HBVr, however, the risk of HBVr in patients undergoing non-TNF-targeted biologics have not been fully understood. In this review, we discuss the risk of HBVr in patients treated with non-TNF-targeted biologics, and immunological mechanisms of these medications causing HBVr.

Keywords: Autoimmune diseases; Biological therapy; Hepatitis B virus; Interleukin-17; Interleukin-23; Janus kinases.

Figure 1

The possible immunological mechanism to explain how non-tumor necrosis factor-targeted biologics can induce the development of hepatitis B reactivation. cccDNA: Covalently closed circular DNA; HBV: Hepatitis B virus; IFN: Interferon; IL: Interleukin; T_H17 cells: IL-17 producing T helper cells; T_H1 cells: T helper 1 cells; Tc cells: Cytotoxic T cells.