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Hepatology. 2018 Aug 31. doi: 10.1002/hep.30243. [Epub ahead of print]
HBV-specific T cells as a Biomarker for Discontinuation of Nucleos(t)ide Analogue Therapy for Chronic Hepatitis B.
Tian Y1, Ou JJ2.
Author information
1
Department of Pathology and Laboratory Medicine, Los Angeles County and University of Southern California Medical Center, Los Angeles, California.
2
Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California.
Abstract
Hepatitis B virus (HBV) can cause severe liver diseases and is a major health problem. It chronically infects approximately 250 million people worldwide. Nucleos(t)ide analogs (NUCs), including lamivudine, adefovir, entecavir, tenofovir and telbivudine, are the most frequently used drugs for treating chronic hepatitis B (CHB) patients. NUCs can efficiently suppress HBV DNA replication and reduce viral load, leading to the loss of the HBV e antigen (HBeAg), the appearance of antibodies against HBeAg, and the normalization of the alanine aminotransferase (ALT) level. However, they cannot target the HBV genomic DNA, also known as the covalently closed circular DNA (cccDNA), in infected hepatocytes. For that reason, the discontinuation of the NUC therapy can lead to viral rebound and the development of hepatic flares, and a lifelong treatment of this therapy is often required for CHB patients. Nevertheless, there are also some patients for whom the treatment with NUCs can be safely stopped. Unfortunately, the biomarkers for the identification of this subset of patients are currently lacking. Recently, Rivino et al. found that the population of PD1+ HBV-specific T cells was much higher in chronic HBV patients who successfully discontinued the NUC therapy without developing hepatic flares than in those patients who developed hepatic flares (1). Their finding indicated that PD1+ HBV-specific T cells might serve as the much-needed biomarker for safe discontinuation of the NUC therapy for CHB patients. This article is protected by copyright. All rights reserved.
KEYWORDS:
HBV ; HBV-specific T cells; antiviral therapy; biomarkers; nucleos(t)ide analogues
PMID:
30168616
DOI:
10.1002/hep.30243
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