Pamela Ruvalcaba-Hernández, Minerva Mata-Rocha, Ernesto Cruz-Muñoz Mario, Manuel Mejía-Aranguré Juan, Norberto Sánchez-Escobar, Francisco Arenas-Huertero, de la Torre Silvia Melchor-Doncel, Angélica Rangel-López, Elva Jiménez-Hernández, Carlos Nuñez-Enriquez Juan, Sara Ochoa, Juan Xicohtencatl-Cortes, Ariadnna Cruz-Córdova, Paula Figueroa-Arredondo, José Arellano-Galindo
Laboratorio de Virología, Unidad de Investigación en Enfermedades Infecciosas, Hospital Infantil de México Federico Gómez, Mexico City 06720, Mexico.
Posgrado en Ciencias Biológicas, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.
Viruses. 2025 Mar 18;17(3):435. doi: 10.3390/v17030435.
Leukemia is a hematologic malignancy; acute lymphoblastic leukemia (ALL) is the most prevalent subtype among children rather than in adults. family members produce proteins during latent infection phases that may contribute to cancer development. One such protein, viral interleukin-10 (vIL-10), closely resembles human interleukin-10 (IL-10) in structure. Research has explored the involvement of human cytomegalovirus (hCMV) in the pathogenesis of ALL. However, the limited characterization of its latent-phase proteins restricts a full understanding of the relationship between hCMV infection and leukemia progression. Studies have shown that hCMV induces an inflammatory response during infection, marked by the release of cytokines and chemokines. Inflammation may, therefore, play a role in how hCMV contributes to oncogenesis in pediatric ALL, possibly mediated by latent viral proteins. The classification of a virus as oncogenic is based on its alignment with cancer's established hallmarks. Viruses can manipulate host cellular mechanisms, causing dysregulated cell proliferation, evasion of apoptosis, and genomic instability. These processes lead to mutations, chromosomal abnormalities, and chronic inflammation, all of which are vital for carcinogenesis. This study aims to investigate the role of vIL-10 during the latent phase of hCMV as a potential factor in leukemia development.
白血病是一种血液系统恶性肿瘤；急性淋巴细胞白血病（ALL）在儿童中比在成人中更为常见。家庭成员在潜伏感染阶段会产生可能导致癌症发展的蛋白质。其中一种蛋白质，病毒白细胞介素-10（vIL-10），在结构上与人类白细胞介素-10（IL-10）非常相似。研究已经探讨了人类巨细胞病毒（hCMV）在ALL发病机制中的作用。然而，对其潜伏阶段蛋白质的有限表征限制了对hCMV感染与白血病进展之间关系的全面理解。研究表明，hCMV在感染期间会引发炎症反应，其特征是细胞因子和趋化因子的释放。因此，炎症可能在hCMV如何促进小儿ALL的肿瘤发生中起作用，可能是由潜伏性病毒蛋白介导的。将一种病毒归类为致癌病毒是基于它与癌症已确定的特征的一致性。病毒可以操纵宿主细胞机制，导致细胞增殖失调、逃避细胞凋亡和基因组不稳定。这些过程会导致突变、染色体异常和慢性炎症，所有这些对于致癌作用都至关重要。本研究旨在探讨vIL-10在hCMV潜伏阶段作为白血病发展潜在因素的作用。
