A research has found the mechanism behind establishment and maintenance of persistent infection by Hepatitis B virus (HBV). It could help in the development of new therapeutic strategies. HBV is a blood-borne pathogen that chronically infects approximately 350 million people worldwide, and more than 780,000 patients die annually due to HBV related liver diseases. Chronic HBV infection is associated with impaired virus-specific T-cell responses. Myeloid-derived suppressor cells (MDSCs) are immune cells known to play a critical role in impairing anti-viral T-cell responses. In addition, the Hepatitis B e-antigen (HBeAg)- a Hepatitis B viral protein- may represent a viral strategy to establish persistent infection, but the mechanism remains largely unknown. Researchers examined the mechanisms underlying the expansion of myeloid-derived suppressor cells (MDSCs) and the suppression of T-cell responses in persistent HBV infection. The researchers analysed the circulation frequency of MDSCs in 164 patients with chronic HBV infection and 70 healthy donors. They found that the frequency of circulating MDSCs in HBeAg-positive patients is higher than in HBeAg-negative patients. The findings suggest a novel mechanism in which HBeAg-induced MDSC expansion impairs T-cell function through the IDO pathway and favours the establishment of persistent HBV infection. The HBeAg-MDSC-IDO axis may, therefore, serve as an immunotherapeutic target of chronic hepatitis B.