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Review
. 2025 May 10;14(1):69.
doi: 10.1186/s40164-025-00655-2.

Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling

Qing Xiao #  1 , Yi Liu #  1 , Xuejiao Shu #  1 , Ya Li #  1 , Xiaomei Zhang  1 , Chaoyu Wang  1 , Sanxiu He  1 , Jun Li  1 , Tingting Li  1 , Tingting Liu  1 , Yao Liu  2
Affiliations
Review

Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling

Qing Xiao et al. Exp Hematol Oncol. .

Abstract

Haematological malignancies are one of the most common tumors, with a rising incidence noted over recent decades. Viral infections play significant roles in the pathogenesis of these malignancies globally. This review delves into the contributions of various known viruses-specifically Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), human T-cell leukemia virus type 1 (HTLV-1), Kaposi's sarcoma-associated herpesvirus (KSHV), human cytomegalovirus (HCMV), hepatitis B virus (HBV), hepatitis C virus (HCV), and human papillomavirus (HPV)-in the development of haematological malignancies. These viruses are shown to drive tumorigenesis through mechanisms, such as metabolic reprogramming, epigenetic modifications, and remodeling of the immune microenvironment. By directly disrupting fundamental cellular functions and altering metabolic and epigenetic pathways, these viruses foster an immune milieu that supports both viral persistence and tumor growth. A thorough understanding of these viral oncogenic processes is crucial not only for etiological discovery but also for developing targeted interventions. This review emphasizes the need for continued research into the specific ways these viruses manipulate the host cell's metabolic and epigenetic environments, aiming to provide insights that could guide future advancements in treatment modalities.

Keywords: Epigenetic regulation; Haematological malignancies; Immune microenvironment; Metabolism; Oncogenic viruses.

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Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
EBV-encoded latent proteins and infection mechanisms. (A) EBV-infected cells express several latent antigens, including EBV nuclear antigens and latent membrane proteins. (B) EBV infections are classified as latent or lytic. EBV can periodically transition to the lytic cycle, leading to viral replication, shedding and subsequent dissemination. This figure was created with BioRender.com
Fig. 2
Fig. 2
Molecular mechanisms of EBV oncogenesis in haematological malignancies. EBV infection acts as a tumorigenic factor through metabolic reprogramming, epigenetic modification, and immune microenvironment remodeling. This figure was created with BioRender.com
Fig. 3
Fig. 3
Molecular mechanisms of KSHV oncogenesis in haematological malignancies. KSHV infection acts as a tumorigenic factor through metabolic reprogramming, epigenetic modification, and immune microenvironment remodeling. This figure was created with BioRender.com
Fig. 4
Fig. 4
Molecular mechanisms of HTLV-1 oncogenesis in haematological malignancies. HTLV-1 infection acts as a tumorigenic factor through metabolic reprogramming, epigenetic modification, and immune microenvironment remodeling. This figure was created with BioRender.com
Fig. 5
Fig. 5
HIV-1 genome and infection mechanism. (A) HIV is an enveloped virus encoding three polyproteins (Gag, Pol, and Env) and six accessory proteins (Tat, Rev, Nef, Vpr, Vif, and Vpu); (B) HIV invades host cells and replicates its genetic material through a complex series of steps, a process that involves binding, fusion, DNA synthesis, integration, and the production of new virus particles using host cell surface receptors. This figure was created with BioRender.com
Fig. 6
Fig. 6
Molecular mechanisms of HIV oncogenesis in haematological malignancies. HIV infection acts as a tumorigenic factor through metabolic reprogramming, epigenetic modification, and immune microenvironment remodeling. This figure was created with BioRender.com
See this image and copyright information in PMC

References

    1. Moore PS, Chang Y. Why do viruses cause cancer? Highlights of the first century of human tumour virology. Nat Rev Cancer. 2010;10(12):878–89. - DOI - PMC - PubMed
    1. Bouvard V, Baan R, Straif K, Grosse Y, Secretan B, El Ghissassi F, et al. A review of human carcinogens--Part B: biological agents. Lancet Oncol. 2009;10(4):321–2. - DOI - PubMed
    1. Bouvard V, Baan RA, Grosse Y, Lauby-Secretan B, El Ghissassi F, Benbrahim-Tallaa L, et al. Carcinogenicity of malaria and of some polyomaviruses. Lancet Oncol. 2012;13(4):339–40. - DOI - PubMed
    1. Beachy PA, Karhadkar SS, Berman DM. Tissue repair and stem cell renewal in carcinogenesis. Nature. 2004;432(7015):324–31. - DOI - PubMed
    1. Hatano Y, Fukuda S, Hisamatsu K, Hirata A, Hara A, Tomita H. Multifaceted interpretation of Colon cancer stem cells. Int J Mol Sci. 2017;18(7). - PMC - PubMed

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