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Updated: Dec 30, 2025

Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis
Published on: September 7, 2022
Differences in Epstein-Barr Virus Characteristics and Viral-Related Microenvironment Could Be Responsible for
Aldana Vistarop1, Oscar Jimenez1, Melina Cohen1
1Multidisciplinary Institute for Investigation in Pediatric Pathologies (IMIPP), CONICET-GCBA. Molecular Biology Laboratory, Pathology Division, Ricardo Gutiérrez Children's Hospital, Buenos Aires C1425EFD, Argentina.
Insights
Epstein-Barr virus (EBV) infection in young children is linked to Hodgkin lymphoma (HL). Research shows specific EBV proteins and immune cells in pediatric HL, suggesting a role in lymphomagenesis.
Area of Science:
- Pediatric Oncology
- Virology
- Immunology
Background:
- Epstein-Barr virus (EBV) presence correlates with Hodgkin lymphoma (HL) in young Argentinian children.
- Hodgkin lymphoma originates from germinal centers (GC), suggesting a link between EBV and GC biology.
Purpose of the Study:
- To compare EBV protein expression and microenvironment markers in pediatric HL patients versus EBV-positive germinal centers (GC) in children.
- Investigate the role of EBV in pediatric Hodgkin lymphoma pathogenesis.
Main Methods:
- In situ hybridization and immunohistochemistry (IHC) were used to assess EBV presence and immune cell markers.
- Analysis focused on viral latency patterns, protein co-expression (LMP1, LMP2), and immune cell infiltration (CD4+, IL10, CD68+).
Main Results:
- Viral latency II pattern was observed in all pediatric HL patients and most EBV+ GCs.
- LMP1 and LMP2 co-expression was significantly higher in HL cases compared to EBV+ GCs.
- Increased CD4+, IL10, and CD68+ cells were found in EBV+ GCs, with higher IL10+ cells in EBV+ HL patients.
Conclusions:
- LMP1 expression might be sufficient for neoplastic transformation in EBV-associated HL.
- An immune-regulatory environment may counteract cytotoxic effects in EBV-associated HL.
- CD4+ and CD68+ cells could collaboratively restrict EBV-mediated lymphomagenesis in tonsillar GCs.
Abstract:
In Argentina, Epstein-Barr virus (EBV) presence is associated with Hodgkin lymphoma (HL) in patients younger than 10 years, suggesting a relationship between low age of EBV infection and HL. Given that HL is derived from germinal centers (GC), our aim was to compare EBV protein expression and microenvironment markers between pediatric HL patients and EBV+GC in children.
Methods:
EBV presence and immune cell markers were assessed by in situ hybridization and immunohistochemistry (IHC).
Results:
Viral latency II pattern was proved in all HL patients and in 81.8% of EBV+ tonsillar GCs. LMP1 and LMP2 co-expression were proved in 45.7% HL cases, but only in 7.7% EBV+ GC in pediatric tonsils. An increase in CD4+, IL10, and CD68+ cells was observed in EBV+ GC. In pediatric HL patients, only the mean of IL10+ cells was statistically higher in EBV+ HL.
Conclusions:
Our findings point us out to suggest that LMP1 expression may be sufficient to drive neoplastic transformation, that an immune regulatory milieu counteracts cytotoxic environment in EBV-associated Hodgkin lymphoma, and that CD4+ and CD68+ cells may be recruited to act in a local collaborative way to restrict, at least in part, viral-mediated lymphomagenesis in tonsillar GC.
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