# 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

PMC · DOI: 10.3390/v17030435 · Viruses · 2025-03-18

## TL;DR

This paper investigates whether a protein from cytomegalovirus, vIL-10, could be linked to the development of childhood leukemia.

## Contribution

The study explores the potential role of the latent-phase vIL-10 protein in contributing to acute lymphoblastic leukemia pathogenesis.

## Key findings

- vIL-10 from hCMV is structurally similar to human IL-10 and may influence inflammation during infection.
- Latent-phase viral proteins like vIL-10 could contribute to oncogenesis through chronic inflammation and genomic instability.
- Understanding hCMV's latent proteins may improve understanding of leukemia development in children.

## Abstract

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.

## Linked entities

- **Proteins:** VILL (villin like), IL10 (interleukin 10)
- **Diseases:** acute lymphoblastic leukemia (MONDO:0004967), leukemia (MONDO:0004355)

## Full-text entities

- **Genes:** IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}
- **Diseases:** hematologic malignancy (MESH:D019337), cancer (MESH:D009369), chromosomal abnormalities (MESH:D002869), ALL (MESH:D054198), Inflammation (MESH:D007249), Leukemia (MESH:D007938), infection (MESH:D007239), carcinogenesis (MESH:D063646)
- **Species:** Homo sapiens (human, species) [taxon 9606], Human betaherpesvirus 5 (no rank) [taxon 10359], Cytomegalovirus (genus) [taxon 10358]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11945621/full.md

## References

141 references — full list in the complete paper: https://tomesphere.com/paper/PMC11945621/full.md

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Source: https://tomesphere.com/paper/PMC11945621