Abstract
BackgroundTreatment with nucleotide analogs is known to be effective in inhibiting HBV replication; however, patients with chronic hepatitis B (CHB) often show a wide range of clinical responses to these drugs. Therefore, the identification of an early immunologic marker associated with the clinical outcomes in such cases is critical for the improved clinical management. In our study, we aimed to investigate whether the viral load in CHB patients affected the ratio of the number of regulatory T cells (Tregs) to the number of interleukin-17-producing helper (Th17) cells. Further, we evaluated the clinical implications of the alterations in this ratio.Methodology/Principal FindingsNine patients seropositive for hepatitis B e antigen received entecavir monotherapy for 12 months and the percentages of Tregs and Th17 cells as well as the HBV-specific IL-17 productions in these patients were longitudinally analyzed. The entecavir-induced suppression of HBV replication was accompanied by a rapid increase in the number of Th17 cells, together with a decrease in Treg cells, which lead to a significant reduction of Treg/Th17 ratios. In addition, peripheral blood mononuclear cells (PBMCs) exhibited a decreased IL-17 production upon stimulation with the HBV core antigen in vitro.ConclusionsThe inhibition of viral replication results in an increase in Th17 cells and concomitant decrease in Treg cells. This imbalance of Treg cells to Th17 cells might have an important role in HBV persistence during entecavir treatment.
Highlights
Patients who are chronically infected with hepatitis B virus (HBV) are at a risk of developing liver cirrhosis and hepatocellular carcinoma owing to many factors
The inhibition of viral replication results in an increase in the number of interleukin-17-producing helper (Th17) cells and concomitant decrease in Treg cells. This imbalance of Treg cells to Th17 cells might have an important role in HBV persistence during entecavir treatment
We aimed to investigate the influence of the decrease in the viral load on the percentages of Tregs and Th17 cells, and thereby assess the effectiveness of antiviral therapy in chronic hepatitis B (CHB) patients
Summary
Patients who are chronically infected with hepatitis B virus (HBV) are at a risk of developing liver cirrhosis and hepatocellular carcinoma owing to many factors. Antiviral treatment with nucleos(t)ide analogs is one of the therapeutic options for patients with chronic hepatitis B (CHB) These drugs effectively suppress HBV replication, alleviate liver injury, and decelerate disease progression. The identification of an early immunologic marker associated with the clinical outcomes of the antiviral therapy is critical for the development of improved clinical management and therapeutic options. Treatment with nucleotide analogs is known to be effective in inhibiting HBV replication; patients with chronic hepatitis B (CHB) often show a wide range of clinical responses to these drugs. We evaluated the clinical implications of the alterations in this ratio
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