Background: The patient's immune response is one of the major factors infl uencing HBV eradication or chronifi cation, and it is thought to be responsible for the treatment success. Aim: Our study aimed to investigate whether cellular defense mechanisms are associated with the course of HBV infection (spontaneous recovery [SR] or chronifi cation [CHB]) and with the therapeutic approach. Patients and methods: A total of 139 patients (118 with CHB, 21 SR) and 29 healthy individuals (HI) were immunophenotyped by fl owcytometry. Fifty-six patients were treatment-naïve, 20 were treated with interferons and 42 with nucleoside/nucleotide analogues. Results: Defi ciency of T lymphocytes, helper-inducer (CD3+CD4+), suppressorcytotoxic (CD8+CD3+) and cytotoxic (CD8+CD11b-, CD8+CD28+) subsets, activated T cells (CD3+HLA-DR+, CD8+CD38+) and increased CD57+CD8-cells, elevated percentages of B lymphocytes and NKT cells were observed in CHB patients compared with HI. In SR patients, elevated CD8+CD11b+, NKT and activated T cells were found in comparison with controls. The higher values of T cells and their subsets in SR patients than in CHB patients refl ect a recovery of cellular immunity in resolved HBV infection individuals. In both groups of treated patients, reduced T lymphocytes, CD3+CD4+ and CD8+CD38+ subsets were found in comparison with HI. Higher proportions of cytotoxic subsets were observed in treated patients compared with treatment-naïve CHB patients, more pronounced in the group with interferon therapy. Conclusion: Our data demonstrate that cellular immune profi les may be of prognostic value in predicting the clinical course of HBV infection, and the determination of the therapeutic response.

INTRODUCTION:The immune response in the Hepatitis B virus (HBV) represents a key factor in the infection outcome. However, the relation between the viral replication and the host immune reactivity is still a matter of investigation.AIM: To investigate whether the cellular immune response of newly diagnosed and treatment naïve chronic hepatitis B (CHB) patients may be influenced by the replicative status of HBV. MATERIALS AND METHODS:A total of 45 (17 female and 28 male) newly diagnosed untreated CHB patients aged 42.48±13.19 years (19÷71 years) were enrolled in this study. The patients were divided into two groups according to the viral load: >0÷≤10 4 copies/ml (n=25) and >10 4 ÷<10 8 copies/ml (n=17). Flow cytometric immunophenotyping was performed for evaluation of the cellular immunity. Serum HBV DNA load was assessed by quantitative real-time polymerase chain reaction. RESULTS: Similar alterations were observed in both patients' groups in comparison to the healthy controls. It could be summarized as it follows: decreased total T cells (CD3+) due to low helper-inducer (CD3+CD4+) and suppressor-cytotoxic (CD3+CD8+) subpopulations; reduced effector cytotoxic (CD8+CD11b-; CD8+CD28+) and activated (CD3+HLA-DR+, CD8+CD38+) T-cell subsets; increased CD57+CD8-cells; elevated percentage of B lymphocytes. No significant differences in the studied immune parameters were detected between both patients' groups except the significantly elevated CD4/CD8 ratio in individuals with higher in comparison to those with lower HBV DNA levels. CONCLUSION: Alterations in the cellular immune response of CHB patients were observed resulting mainly in significantly decreased T-cell subpopulations, particularly those with effector cell immune phenotype regardless of the viral load.