CD19 gene Polymorphism in Chronic Myeloid Leukemia Patients Infected with Varicella Zoster Virus

Background: Chronic myeloid leukemia (CML), driven by the BCR-ABL1 oncogene, is associated with immune dysregulation and increased susceptibility to reactivation of viruses such as Varicella Zoster Virus (VZV). CD19, a critical B cell receptor co-regulator, may influence the immune response in CML. Objective: This study investigates CD19 polymorphisms and their potential link to VZV reactivation in patients with CML. Methodology: Blood samples from 120 CML patients and 100 age-and sex-matched healthy controls (AHC) were analyzed. CD19 serum levels were quantified using ELISA. CD19 genotyping (AA, AG, and GG) and VZV-DNA detection were performed by PCR and sequencing in both CML patients and healthy controls. Statistical analyses included Chi-square, Hardy-Weinberg equilibrium, and Spearman’s correlation (SPSS v24). Results: CD19 levels were significantly lower in CML patients (27.45 ± 16.23 pg/mL) versus controls (37.47 ± 40.43 pg/mL; p=0.02). Genotyping revealed a higher GG genotype frequency in CML (30% vs. 10% in controls), although no significant association was found (p=0.21). VZV DNA was not detected in any of the samples. CD19 levels and polymorphisms were correlated with patient age (r=0.647, p=0.04; r=0.722, p=0.03). No significant differences in biochemical parameters were observed, except for elevated creatinine levels in the relapsed patients (p=0.01). Conclusions: Reduced CD19 levels in patients with CML suggest immune dysregulation, potentially impairing B-cell function. The absence of VZV reactivation contrasts with previous studies, possibly because of effective antiviral management or limited sample diversity. CD19 polymorphisms, particularly the GG genotype, may warrant further investigation as biomarkers of immune status in CML. These findings underscore the need for larger studies to clarify CD19’s role in viral susceptibility and therapeutic outcome.