Abstract
The hepatitis B virus (HBV) exhibits a pronounced lymphotropic potential, but its role in the pathogenesis of lymphoproliferative disorders remains insufficiently characterized. A comprehensive investigation of the molecular-genetic and immunological mechanisms governing virus-target cell interactions is required to inform preventive and therapeutic strategies. We performed an analysis of original studies, meta-analyses and systematic reviews indexed in PubMed, eLIBRARY.RU and CyberLeninka, as well as in international bibliographic and full-text resources such as Wiley Online Library, BioMed Central (BMC), and HighWire Press, using relevant keywords. From the reviewed literature, evidence supports the capacity of HBV to persist in hematopoietic progenitor cells of the bone marrow, thereby establishing a long-lived extrahepatic viral reservoir. Key oncogenic mechanisms were delineated: integration of viral DNA into the host genome, resulting in genomic instability and structural rearrangements; functional activity of the viral oncoprotein HBx, which modulates signaling and epigenetic regulators; and immune dysfunction induced by chronic antigenic stimulation, characterized by T-cell exhaustion and systemic dysregulation of immune responses. Clinical data indicate that HBV-associated lymphomas exhibit distinctive features — an aggressive clinical course, a specific mutational landscape, and reduced responsiveness to standard therapeutic regimens. Conclusions. The pathogenesis of HBV-associated lymphoproliferative disorders is multifactorial, driven by the interplay of viral, genomic, and immune factors, which underlie their aggressive clinical course and unfavorable prognosis.