HBV and Lymphoma

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Background

Hepatitis B virus (HBV) infection is a global public health problem, with the highest prevalence observed in Asia, Africa and South America. Over 257 million people are infected worldwide and 887,000 deaths are caused directly or indirectly by HBV every year. Even in the US and Europe, both non-endemic regions, approximately 1 and 13 million individuals have a chronic HBV infection respectively.

HBV is a common risk factor for the development of hepatocellular carcinoma and epidemiological and clinical studies have also shown that infection may increase the incidence of several types of B-cell lymphoma. In particular, individuals infected with HBV have a two- to threefold higher risk of developing non-Hodgkin lymphomas (NHL), including diffuse large B-cell lymphoma (DLBCL). Despite this, analyses of specific subtypes of NHL have yielded inconsistent results. The association between HBV infection and NHL has been demonstrated for HBsAg-positive patients, although patients with occult HBV infection have been shown to also be at higher risk of NHL. Meta-analyses confirmed this association, regardless of the region and endemicity of HBV; however, only a few studies have analyzed the characteristics of HBV-associated NHL in low-endemicity regions. In addition, few studies focus on the impact of antiviral prophylaxis for DLBCL patients with HBV infection. It has been suggested that HBV therapy could also positively impact on the natural history of the lymphoproliferative disorder.

The etiological role of HBV in lymphomagenesis remains largely unknown. HBV can directly infect lymphocytes and integrate its nucleic acid sequences into the host’s genome, leading to the overexpression of oncogenes or the downregulation of tumor suppressor genes. Indeed, patients with NHL and HBV infection have had the virus detected in their peripheral blood mononuclear cells, in which HBV viral integration has also been observed. Furthermore, HBV viral replication and viral antigens may stimulate the expression, production and release, of hematopoietic tumor growth factors, leading to clonal lymphocyte proliferation.

Patients with lymphoma and current (positive hepatitis B surface antigen (HBsAg)) or past (positive hepatitis B core antibody (HBcAb) and negative HBsAg) exposure to HBV infection who receive chemotherapy, immunosuppressive therapies and steroids, may develop an HBV reactivation (HBVr) infection, potentially leading to interruption of chemotherapy and subsequently a significant increase in morbidity (e.g. hepatitis flare, hepatic decompensation, and hepatic failure) and mortality. The highest rates of HBVr are typically observed during immuno-chemotherapy with the anti-CD20 monoclonal antibody, rituximab, in particular when it is combined with cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy. Chimeric antigen receptor (CAR) T-cell therapy is a safe and effective therapy of B-cell neoplasms, but it is unknown whether current or prior HBV-infection impacts the safety and efficacy of CAR T-cell therapy.

All patients with lymphoma and current or past HBV infection who receive chemo-immunotherapy, should receive anti-HBV drugs as prophylaxis. The lack of reliable biologic markers of immune recovery prevents the definition of the optimal duration of prophylaxis and the incidence of delayed HBV reactivation after the cessation of antiviral prophylaxis in lymphoma patients is unknown. There is a great need for high-quality studies that provide clear indications on the duration of HBV prophylaxis in either HBsAg-positive or anti-HBc-positive patients receiving chemo-immunotherapy and on the duration of HBV DNA monitoring after withdrawal of antiviral therapy. Studies regarding the possible protective effect of anti-HBV vaccine against lymphomas are also lacking.

In this collection, we will collate Original Research, Review, and Mini-Review articles encompassing basic science, translational research, and epidemiological studies that focus on but are not limited to:
- Mechanisms underlying the oncogenic role of HBV in lymphomagenesis, and the the association between HBV infection and lymphomas
- HBV lymphotropism and its significance with respect to HBV biology, persistence and the pathogenesis of lymphomas
- The impact of antiviral prophylaxis on the natural history of lymphoma and its underlying mechanisms in patients with active or past HBV infection
- The impact of HBV infection on treatment outcomes and survival of patients with lymphoma
- The effect of antiviral therapy on HBV reactivation in patients with lymphoma undergoing chemo-immunotherapy
- HBV reactivation in patients with lymphoma: duration of therapy, monitoring and optimal markers to guide discontinuation of antiviral therapy
- Existing and novel viral markers in the management of patients with HBV and lymphoma
- The risk of HBV reactivation after CAR T-cell therapy
- Antiviral prophylaxis after CAR T-cell therapy in patients with past or chronic HBV infection
- The possible protective effect of the hepatitis B vaccine against lymphomas

Please note: manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.

Keywords: Lymphoma, HBV, CAR-T therapy, HBV vaccine, HBV lymphomagenesis, viral markers, prevention HBV reactivation, Hepatitis B virus

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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