The aim of this study was to determine the correlation between dynamic changes in serum cytokine/chemokine expression levels in response to entecavir (ETV) treatment and HBV e antigen (HBeAg) seroconversion in patients with chronic hepatitis B (CHB). Four cytokines (interleukin [IL]-4, IL-6, IL-8, and interferon-γ) and five chemokines (macro-phage inflammatory protein [MIP]-1α, MIP-1β, platelet derived growth factor-BB, and interferon-inducible protein 10 [IP-10]) before ETV therapy and at 3, 6, 12, 24, 36 and 60 months during therapy in 105 CHB patients were analyzed. The results showed that the low decrease rate of IP-10 levels after 1 year of ETV treatment was an independent predictor of HBeAg seroconversion at year 5 (Hazard ratio = 0.972). The area under the receiver operating characteristic curves for the decrease rate of IP-10 levels after 1 year of treatment to discriminate a year-5 HBeAg seroconversion was 0.752 (p = 0.005). The results indicate that higher IP-10 level at year one of ETV treatment is associated with an increased probability of HBeAg seroconversion. Quantification of IP-10 during ETV treatment may help to predict long-term HBeAg seroconversion in patients with CHB.
This study aimed to determine the degree of clonal expansion of T cells in peripheral blood mononuclear cells (PBMCs) isolated from patients suffering from different clinical types of hepatitis B (HB) infection and to analyse the clinical relevance of the skewed T-cell receptor beta variable (TCRBV). Sera and PBMCs were collected from 90 HB patients. Gene melting spectral pattern (GMSP) analysis was used to determine the distribution and expansion of populations expressing specific TCRBV complementary determined region 3 (CDR3) genes. TCRBV genes associated with monoclonal expansion were sequenced. TCRBV families from the majority of patients (80/90) displayed skewed T-cell expansion. Furthermore, TCRBV11, BV12 and BV13.1 were more frequent than other TCRBV genes; the sequence of TCRBV11 CDR3 was expressed as 'VYNEQ' in all patients and was accompanied by the BJ2.1 fragment. In patients with chronic HB, the frequency of skewed TCRBV was inversely correlated with hepatitis B virus (HBV) DNA levels. The persistently skewed TCRBV gene families in HB patients may be associated with the development and maintenance of hepatitis. GMSP analysis of TCRBV gene families may be helpful in estimating disease status, and BV11 may be associated with HBV replication in patients with chronic HBV infection.
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