EAN 2025 | The EnvIMS study: childhood infections and their impact on multiple sclerosis onset in adults

We know very well that the Epstein-Barr virus is a risk factor for multiple sclerosis, but the role of other common virus-related infections is less understood. Our study was aimed at investigating whether childhood infections like measles, mumps, rubella, and chickenpox could affect the risk of MS and if they affect also the age at MS onset. We used the data collected within the EnvIMS study, which is a large multinational case-controlled and population-based study. We used data from Italian and Norwegian populations. Data have been collected through the Envim questionnaire. Participants self-reported through the questionnaire if they contracted measles, mumps, rubella, or chickenpox during their childhood. We calculated the adjusted odds ratio, considering also some covariates like smoking habit, infectious mononucleosis, and low sun exposure. We also assessed with ANCOVA the relationship between multiple sclerosis age at onset and viral infections. We found that multiple sclerosis risk was not increased by viral infections in both populations, but as for the secondary aims, we discovered that measles was associated with later MS onset, both in Italy and in Norway. As for mumps, it was associated with a later MS onset only in Norway. Rubella instead was linked to an earlier MS onset in Italian men, but with a later MS onset among Norwegian women. Finally, chickenpox was found to be associated with an earlier MS onset in both populations with strong significant results. In conclusion, we suggest with our study that childhood infections may affect MS course, not MS risk per se, but probably the age at MS onset. Measles in particular seems to delay the onset of the disease, which has never been proven before, while instead chickenpox seems to anticipate the onset of the disease. This result in particular may align with the results of a study published in 2023, which is a Mendelian randomization genetic study suggesting the existence of a shared immune-related mechanism between varicella and multiple sclerosis. I must acknowledge some limitations of our study, which in particular is the recall bias, as the infectious history was self-reported by all the subjects. In the future, some research using longitudinal prospective design and also serological markers will help us to better understand the association between childhood infections and the risk of multiple sclerosis and if they may have an impact on the multiple sclerosis course and progression.

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