Abstract

The Non-Hodgkin Lymphoma (NHL) is a heterogeneous group of malignancies ranked as the most common haematological cancer worldwide, more than 544 000 new cases being reported in 2020. More recent epidemiological studies have shown an increased risk of several types of B-cell Lymphoma development, the most prevalent being diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) subtypes, in patients infected with hepatitis B virus (HBV). These patients are more difficult to treat and their survival rate is lower compared to uninfected people. HBV is known as a hepatotropic virus, although viral HBV-DNA has been identified in extrahepatic tissues, such as kidney, pancreas or peripheral blood mononuclear cells (PBMC). However, the mechanistic relationship between HBV infection and lymphoid cancer is not known. Preliminary data have shown that NTCP, the specific HBV receptor is expressed in normal B cells. After exposure to HBV viral particles, B cells become capable of producing viral core antigens (HBcAg). Antiviral roles and/or cancer-promotion functions in B-cells of APOBEC3 deaminases overexpression remain to be determined.

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