Peripheral blood B cell subpopulations in chronic hepatitis B and C virus infections
Abstract
Chronic infections caused by hepatitis B virus (HBV) and hepatitis C virus (HCV) remain a significant public health concern. Although T cell exhaustion plays a key role in the immunity behind the disease, B lymphocytes function and distribution in these infections remain poorly understood. The aim of this study was to compare the distribution of major and minor peripheral B cell subsets in patients with chronic hepatitis C (CHC) and chronic hepatitis B (CHB). The study included 39 patients with CHC, 28 patients with CHB, and 30 healthy donors. The B cell (CD19+) subpopulation composition was evaluated with flow cytometry based on the expression of CD5, CD27, and CD38. Statistical analysis was performed with nonparametric tests. The total number of CD19+B cells did not differ between the groups. However, in both patient cohorts, we observed a significant decrease in the relative and absolute proportions of B1 cells (CD5+) compared to the healthy donors (p 0.0001 for both), accompanied by a compensatory increase in B2 cells (CD5-). The share of mature activated B cells (CD27+CD38+) was lower in both CHC and CHB patients (p = 0.0142 and p = 0.0014, respectively). Plasmablast counts (CD27++CD38++) decreased in both groups, with the most pronounced reduction observed in CHB patients (p 0.0001 vs. controls). Transitional B cells (CD27-CD38++) significantly decreased in CHB patients, both in relative and absolute values (p 0.0001 vs. CHC, p = 0.0134 vs. controls). No statistically significant changes were found in the proportions of mature naive cells, memory cells, or double-negative (DN) cells. Chronic HBV and HCV infections are associated not with a quantitative B cell deficiency but with a subpopulation redistribution, demonstrated by a reduction in B1 cells, mature activated B cells, and plasmablasts. A specific hallmark of CHB is the decrease in transitional B cells, which may indicate impairments in the early stages of B cell maturation. Our findings highlight the importance of analyzing minor cell subsets for a better understanding of pathological processes behind of chronic viral hepatitis.