Distinct Inflammatory Imprint in Non-Cirrhotic and Cirrhotic Patients Before and After Direct-Acting Antiviral Therapy.

Background/aims: Hepatitis C virus (HCV) infection remains a global health challenge, leading to chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC). Despite the high efficacy of direct-acting antiviral (DAA) therapy in achieving sustained virologic response (SVR), concerns persist regarding long-term immune alterations and residual risks, particularly in cirrhotic patients.

Methods: This study investigates 75 soluble immune mediator (SIM) profiles in 102 chronic HCV patients, stratified by cirrhosis status, at therapy initiation, end of treatment, and long-term follow-up (median 96 weeks).

Enhancing HBV-specific T cell responses through a combination of epigenetic modulation and immune checkpoint inhibition.

Background And Aims: Chronic HBV infection exhausts HBV-specific T cells, develops epigenetic imprints that impair immune responses, and limits the effectiveness of immune checkpoint inhibitor monotherapy, such as anti-programmed cell death ligand-1 antibody (αPD-L1). This study aimed to determine whether the DNA methyltransferase inhibitor decitabine (DAC) could reverse these epigenetic imprints and enhance immune checkpoint inhibitor efficacy in restoring HBV-specific T cell responses.

Approach And Results: We investigated HBV-specific T cell responses by 10-day in vitro stimulation of peripheral blood mononuclear cells (PBMCs) from patients with chronic HBV infection.