The Epstein-Barr virus (EBV) is a lymphotropic virus which was first discovered from a Burkitt lymphoma cell line in 1964. Investigations estimate that around 90% of the global adult population are infected with EBV. The virus is transmitted via saliva, infects epithelial cells in the oropharynx, replicates and eventually reaches local B-cells where it establishes a latent infection. EBV infection has been associated with a broad range of malignant diseases, in particular Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL). Co-infection with human immunodeficiency virus (HIV) is also common and often corresponds with HIV disease progression and EBV-induced lymphomagenesis. EBV is detected in roughly half of all classic HL cases and is common in patients with Burkitt lymphoma, a subtype of NHL. EBV infection has also been associated with diffuse large B-cell lymphoma (DLBCL), primary central nervous system lymphoma (PCNS), primary effusion lymphoma (PEL) and plasmablastic lymphoma.
Different patterns of latent gene expression have been associated with different lymphomas, for example, HL has been associated with expression of EBNA1, LMP1 and LMP2, expressed during latency II of infection, whilst Burkitt lymphoma is associated with expression of EBNA1, expressed during latency I. Viral transcripts affect multiple signaling pathways and, combined with genetic/epigenetic alterations, contribute to EBV-driven lymphoma.
Further research has demonstrated that EBV may also manipulate the lymphoma microenvironment in favor of lymphoma cell immune escape and proliferation. For example, the interferon response is inhibited by the viral BZLF1 gene and viral DNase/alkaline exonuclease BGLF5 downregulates Toll-like receptors, negatively impacting recognition of pathogen-associated molecular patterns. Expression of an interleukin 10 viral homolog adversely affects the elimination of EBV-infected cells by NK cells. Improving our understanding of how EBV interacts with the immune system may shed light on viral carcinogenesis and present new targets for therapy, such as via immune checkpoint inhibitors.
Great progress has been made in understanding how EBV contributes to the development of different B-cell lymphomas; however, there still remains room to improve the clinical care of patients with EBV-driven lymphomas, such as through early diagnosis, EBV-targeted immunotherapy, and therapies targeting cell pathways modulated by EBV. This collection welcomes manuscripts advancing our understanding of the pathophysiology of EBV-driven lymphoma and the management of patients with EBV-driven lymphoma.
Important 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.
The Epstein-Barr virus (EBV) is a lymphotropic virus which was first discovered from a Burkitt lymphoma cell line in 1964. Investigations estimate that around 90% of the global adult population are infected with EBV. The virus is transmitted via saliva, infects epithelial cells in the oropharynx, replicates and eventually reaches local B-cells where it establishes a latent infection. EBV infection has been associated with a broad range of malignant diseases, in particular Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL). Co-infection with human immunodeficiency virus (HIV) is also common and often corresponds with HIV disease progression and EBV-induced lymphomagenesis. EBV is detected in roughly half of all classic HL cases and is common in patients with Burkitt lymphoma, a subtype of NHL. EBV infection has also been associated with diffuse large B-cell lymphoma (DLBCL), primary central nervous system lymphoma (PCNS), primary effusion lymphoma (PEL) and plasmablastic lymphoma.
Different patterns of latent gene expression have been associated with different lymphomas, for example, HL has been associated with expression of EBNA1, LMP1 and LMP2, expressed during latency II of infection, whilst Burkitt lymphoma is associated with expression of EBNA1, expressed during latency I. Viral transcripts affect multiple signaling pathways and, combined with genetic/epigenetic alterations, contribute to EBV-driven lymphoma.
Further research has demonstrated that EBV may also manipulate the lymphoma microenvironment in favor of lymphoma cell immune escape and proliferation. For example, the interferon response is inhibited by the viral BZLF1 gene and viral DNase/alkaline exonuclease BGLF5 downregulates Toll-like receptors, negatively impacting recognition of pathogen-associated molecular patterns. Expression of an interleukin 10 viral homolog adversely affects the elimination of EBV-infected cells by NK cells. Improving our understanding of how EBV interacts with the immune system may shed light on viral carcinogenesis and present new targets for therapy, such as via immune checkpoint inhibitors.
Great progress has been made in understanding how EBV contributes to the development of different B-cell lymphomas; however, there still remains room to improve the clinical care of patients with EBV-driven lymphomas, such as through early diagnosis, EBV-targeted immunotherapy, and therapies targeting cell pathways modulated by EBV. This collection welcomes manuscripts advancing our understanding of the pathophysiology of EBV-driven lymphoma and the management of patients with EBV-driven lymphoma.
Important 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.
