Is the vIL-10 Protein from Cytomegalovirus Associated with the Potential Development of Acute Lymphoblastic Leukemia?

Bibliographic Details
Title: Is the vIL-10 Protein from Cytomegalovirus Associated with the Potential Development of Acute Lymphoblastic Leukemia?
Authors: Ruvalcaba-Hernández Pamela, Mata-Rocha Minerva, Cruz-Muñoz Mario Ernesto, Mejía-Aranguré Juan Manuel, Sánchez-Escobar Norberto, Arenas-Huertero Francisco, Melchor-Doncel de la Torre Silvia, Rangel-López Angélica, Jiménez-Hernández Elva, Nuñez-Enriquez Juan Carlos, Ochoa Sara, Xicohtencatl-Cortes Juan, Cruz-Córdova Ariadnna, Figueroa-Arredondo Paula, Arellano-Galindo José
Source: Viruses, Vol 17, Iss 3, p 435 (2025)
Publisher Information: MDPI AG, 2025.
Publication Year: 2025
Collection: LCC:Microbiology
Subject Terms: vIL10, ALL (Acute lymphoblastic leukemia), hCMV (Cytomegalovirus), latent proteins, Microbiology, QR1-502
More Details: Leukemia is a hematologic malignancy; acute lymphoblastic leukemia (ALL) is the most prevalent subtype among children rather than in adults. Orthoherpesviridae 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.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1999-4915
Relation: https://www.mdpi.com/1999-4915/17/3/435; https://doaj.org/toc/1999-4915
DOI: 10.3390/v17030435
Access URL: https://doaj.org/article/ac64a1e5d55a4d9aaf6e8e1eb7dc4a6c
Accession Number: edsdoj.64a1e5d55a4d9aaf6e8e1eb7dc4a6c
Database: Directory of Open Access Journals
More Details
ISSN:19994915
DOI:10.3390/v17030435
Published in:Viruses
Language:English