某些称为肿瘤病毒或肿瘤病毒的病毒能够改变组织培养中不同人类或动物细胞类型的基因表达模式，导致不受控制的增殖以及受感染细胞的社会行为的变化：肿瘤病毒转化后，永生化。细胞能够在合适的动物模型中形成恶性肿瘤。目前，有七种人类病毒被归类为不同人类恶性肿瘤的病原体。人类肿瘤病毒的基因组通常编码病毒癌蛋白和非翻译病毒RNA，其影响其靶细胞的基因表达模式或诱导导致肿瘤发生的遗传和表观遗传改变。最近，染色质构象捕获技术和三维（3D）分子成像技术的应用揭示了某些人类肿瘤病毒的基因产物或基因组如何与3D宿主基因组结构相互作用并诱导其改变。本迷你评论旨在涵盖这些发展的选定方面。这些论文进行了简要讨论，描述了如何将 3D 基因组组织者细胞蛋白 CCCTC 结合因子 (CTCF) 的新型病毒结合位点插入到被人类 T 细胞嗜淋巴细胞病毒 1 型 (HTLV-1) 感染的 T 细胞的 DNA 中可能有助于淋巴瘤的发生，以及高风险人乳头瘤病毒基因组整合到宿主细胞 DNA 中如何促进宫颈癌的发生。关于细胞基因组与致癌人类疱疹病毒、EB 病毒 (EBV) 的游离染色质 DNA 基因组相互作用的最新结果也将进行总结，类似于关于游离或整合乙型肝炎病毒 (HBV) DNA 形成的接触的现有数据与宿主染色质。最后，将提出丙型肝炎病毒 (HCV) 诱导染色质改变的假定机制，这可能会解决这个谜题：没有病毒癌基因的细胞质 RNA 病毒如何诱导肝细胞恶性转化。版权所有 © 2023 Minarovits。

Certain viruses called tumor viruses or oncoviruses are capable to change the gene expression pattern of distinct human or animal cell types in tissue culture, resulting in uncontrolled proliferation as well as a change in the social behavior of the infected cells: the oncovirus-transformed, immortalized cells are capable to form malignant neoplasms in suitable animal models. At present, seven human viruses are categorized as causative agents of distinct human malignancies. The genomes of human tumor viruses, typically encode viral oncoproteins and non- translated viral RNAs that affect the gene expression pattern of their target cells or induce genetic and epigenetic alterations contributing to oncogenesis. Recently, the application of chromatin conformation capture technologies and three-dimensional (3D) molecular imaging techniques revealed how the gene products or genomes of certain human tumor viruses interact with and induce alterations in the 3D host genome structure. This Mini Review aims to cover selected aspects of these developments. The papers, discussed briefly, describe how insertion of a novel viral binding site for the 3D genome organizer cellular protein CCCTC-binding factor (CTCF) into the DNA of T cells infected by human T-cell lymphotropic virus type 1 (HTLV-1) may contribute to lymphomagenesis, as well as how integration of high risk human papillomavirus genome into the host cell DNA may facilitate cervical carcinogenesis. Recent results regarding the interactions of cellular genomes with the episomal, chromatinized DNA genomes of oncogenic human herpesvirus, Epstein-Barr virus (EBV) will also be summarized, similarly to available data regarding contacts formed by episomal or integrated hepatitis B virus (HBV) DNA with host chromatin. Finally, a putative mechanism of hepatitis C virus (HCV) induced chromatin alterations will be presented, which may solve the riddle, how a cytoplasmic RNA virus without a viral oncogene could induce malingnant transfrormation of hepatocytes.Copyright © 2023 Minarovits.