Abstract: Non-Hodgkin lymphoma （NHL） is a malignant tumor that occurs in immune cells， including B， T and NK cells. Viral infection， such as infection with Epstein-Barr virus （EBV） and hepatitis virus， plays an important role in the development of NHL. The role and mechanism of hepatitis B virus （HBV） infection in the development and progression of hepatocellular carcinoma through gene integration， mutation， and viral replication have been researched in depth. Mutations induced by apolioprotein B mRNA-editing enzyme catalytic polypeptide （APOBEC） family members are one of the major sources of HBV and host genetic variation， and APOBEC family members act as bridges between HBV-related chronic inflammation and the mutations of HBV and its host genome. Therefore， we suspect that HBV infection plays a significant role in the occurrence of HBV-associated NHL. This review summarizes the role and mechanism of HBV in the occurrence and development of NHL from the aspects of HBV infection， chronic inflammation and immunity， viral variation， signaling pathways， high-frequency mutant genes and epigenetic modification， hoping to provide a theoretical basis for HBV-associated NHL research.