Hepatitis C virus as a trigger for B-cell malignancy

Karyagina M.S., Smakotina S.A., Osyaev N.Yu.

Kemerovo State Medical University, Kemerovo, Russia
Kuzbass Clinical Hospital of Emergency Medical Care named after M.A. Podgorbunsky, Kemerovo, Russia

Hepatitis C virus infection is considered as a systemic disease in which liver damage is combined with extrahepatic disorders affecting the clinical prognosis and quality of life of patients. The article analyzes the role of hepatitis C virus as a risk factor for B-cell lymphoproliferative diseases, including chronic lymphocytic leukemia (CLL). The key mechanisms of lymphooncogenesis are considered: chronic antigenic stimulation of B lymphocytes and direct oncogenic action of viral proteins (Core, NS3) via the CD81 receptor.

A clinical observation is presented, demonstrating that achieving a sustained virological response is not always accompanied by regression of hematological disorders: by the time antiviral therapy begins, a malignant B-cell clone may acquire autonomous properties independent of viral stimulation. The need for long-term dynamic monitoring of patients with HCV infection is emphasized even after virus eradication, in order to timely identify the long-term consequences of infection.