The HIV Environment and Diffuse Large B-cell Lymphoma

^*Correspondence: Mersy Hete, Department of Hematology, Germans Trias i Pujol University Hospital, Universitat Autònoma de Barcelona, Ctra. de Canyet, S/N, 08916 Badalona, Spain, Email:

Keywords

Non-hodgkin lymphoma • HIV • Heterogeneous group • Therapeutic

Introduction

Diffuse Large B-cell Lymphoma (DLBCL) is a heterogeneous group of lymphomas characterized by rapid tumour growth and diverse clinical presentations. This section provides an introduction to DLBCL, its classification, and its association with HIV infection. The incidence of DLBCL is significantly higher in PLWH compared to the general population. This section explores the epidemiological data and highlights the increased risk of DLBCL in the HIVinfected population [1,2]. HIV infection is often accompanied by co-infections, such as Epstein-Barr Virus (EBV) and Human Herpesvirus-8 (HHV-8), which contribute to lymphomagenesis. Chronic inflammation resulting from immune dysregulation also plays a crucial role in DLBCL development. This section discusses the impact of co-infections and chronic inflammation on the pathogenesis of DLBCL.

Literature Review

HIV infection causes progressive immune dysfunction and impairs B-cell surveillance, leading to uncontrolled B-cell activation and proliferation. This section examines the mechanisms by which immune dysregulation contributes to the development of DLBCL. Co-infections with oncogenic viruses, particularly EBV and HHV-8, significantly increase the risk of DLBCL in PLWH. This section explores the role of these viruses in DLBCL pathogenesis and their interaction with HIV. Additional viral co-infections, such as Human Herpesvirus-8 (HHV- 8), hepatitis C virus (HCV), and Human T-cell Lymph Tropic Virus Type 1 (HTLV-1), have been implicated in DLBCL development in PLWH. This section discusses their potential contributions to lymphomagenesis [3-5]. HIV-induced immunodeficiency compromises immune surveillance mechanisms, allowing the expansion of transformed B-cell clones and the escape of malignant cells from immune control. This section discusses the consequences of impaired tumour surveillance in DLBCL development.

Discussion

DLBCL in PLWH often presents at advanced stages and exhibits unique clinical features compared to DLBCL in the general population. This section highlights the clinical characteristics and subtypes of DLBCL in the context of HIV infection. Accurate diagnosis of DLBCL in PLWH is essential for appropriate management. This section discusses the challenges and considerations in histological diagnosis, immunophenotyping, and molecular profiling. DLBCL in PLWH often presents with unique clinical features, including extra nodal involvement, advanced disease stage, and higher rates of central nervous system (CNS) involvement. This section explores the clinical manifestations and subtypes of DLBCL in the HIV setting.

Effective control of HIV replication with Combination Antiretroviral Therapy (CART) has improved overall survival in PLWH. This section discusses the impact of CART on DLBCL outcomes and the importance of incorporating CART in treatment strategies. DLBCL in PLWH is typically treated with standard chemotherapy regimens. This section explores the role of chemotherapy, as well as the emerging use of immunotherapy, in the management of HIVassociated DLBCL [6].

Conclusion

Advancements in understanding the molecular alterations in DLBCL have paved the way for targeted therapies. This section discusses potential targeted therapies and their implications for HIV-associated DLBCL treatment. DLBCL is a significant health concern among PLWH, and the interplay between HIV infection, co-infections, chronic inflammation, and immune dysregulation contributes to its pathogenesis. By elucidating the mechanisms underlying DLBCL development in the HIV environment and implementing appropriate therapeutic approaches, we can improve patient outcomes and enhance the management of DLBCL in this population. Advances in understanding the intricate relationship between the HIV environment and DLBCL have provided valuable insights into the pathogenesis and management of this lymphoma subtype. Further research is needed to elucidate the mechanisms underlying DLBCL development in PLWH, identify novel therapeutic targets, and optimize treatment strategies. By addressing the unique challenges posed by the HIV environment, we can improve outcomes and quality of life for PLWH with DLBCL.

Acknowledgement

None.

Conflict of Interest

None.

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