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Immune response induced by Epstein-Barr virus and Mycobacterium avium subsp. paratuberculosis peptides in current and
G Mameli1, G Madeddu2, D Cossu1
1Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
Background And Purpose:
Infectious mononucleosis (IM) caused by Epstein-Barr virus (EBV) has been associated with increased risk of multiple sclerosis (MS). However, the mechanism linking these pathologies is unclear. Different reports indicate the association of EBV, and recently Mycobacterium avium subsp. paratuberculosis (MAP), with MS. For a better understanding of the role of these pathogens, the host response induced by selected antigenic peptides in subjects with a history of IM that significantly increases the risk of MS was investigated.
Methods:
Both humoral and cell-mediated response against peptides able to induce a specific immune activation in MS patients deriving from lytic and latent EBV antigens BOLF1(305-320), EBNA1(400-413), from MAP MAP_4027(18-32), MAP_0106c(121-132) and from human proteins IRF5(424-434) and MBP(85-98) in subjects with current and past IM were examined.
Results:
EBNA1 and MAP_0106c peptides were able to induce a humoral immune response in subjects with a history of clinical IM in an independent manner. Moreover, these peptides were capable of inducing pro-inflammatory cytokine interferon γ by CD4+ and CD8+ T lymphocytes and interleukin 6 and tumour necrosis factor α by CD14+ monocyte cells.
Conclusion:
Our results highlight that EBV and MAP may be involved independently in the same causal process leading to MS in subjects with a history of IM.
Insights
Infectious mononucleosis (IM) linked to Epstein-Barr virus (EBV) may increase multiple sclerosis (MS) risk. This study found both EBV and Mycobacterium avium subsp. paratuberculosis (MAP) trigger immune responses in IM patients, suggesting independent roles in MS development.
Area of Science:
- Immunology
- Neuroscience
- Microbiology
Background:
- Infectious mononucleosis (IM), caused by Epstein-Barr virus (EBV), is linked to an increased risk of multiple sclerosis (MS).
- The precise mechanisms connecting EBV, and potentially Mycobacterium avium subsp. paratuberculosis (MAP), to MS pathogenesis remain unclear.
- Understanding the host immune response to these pathogens in individuals with a history of IM is crucial for elucidating MS etiology.
Purpose of the Study:
- To investigate the host immune response, both humoral and cell-mediated, to specific antigenic peptides from EBV and MAP.
- To examine immune activation in individuals with a history of IM, a known risk factor for MS.
- To explore the potential independent or combined roles of EBV and MAP in the context of MS development.
Main Methods:
- Assessed humoral and cell-mediated immune responses against selected EBV (BOLF1, EBNA1) and MAP (MAP_4027, MAP_0106c) peptides.
- Included peptides derived from human proteins IRF5 and MBP as controls.
- Analyzed immune responses in subjects with current and past IM.
Main Results:
- EBV's EBNA1 and MAP's MAP_0106c peptides independently induced humoral immune responses in subjects with a history of IM.
- These peptides also triggered pro-inflammatory cytokine production.
- CD4+ and CD8+ T lymphocytes produced interferon-gamma, while CD14+ monocytes produced interleukin-6 and tumor necrosis factor-alpha.
Conclusions:
- Epstein-Barr virus (EBV) and Mycobacterium avium subsp. paratuberculosis (MAP) may independently contribute to the development of multiple sclerosis (MS).
- The immune system's response to specific peptides from both pathogens in individuals with a history of IM highlights their potential roles in MS pathogenesis.
- These findings suggest a complex interplay between infectious agents and host immunity in the etiology of MS.
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