Studies into the mechanism of measles-associated immune suppression during a measles outbreak in the netherlands
ESPID Education. Laksono B. 05/09/19; 263135
Ms. Brigitta Marcella Laksono
Ms. Brigitta Marcella Laksono
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Measles causes a transient immune suppression, leading to increased susceptibility to opportunistic infections. Measles virus (MV) infection of immune cells is facilitated by the cellular receptor CD150. In experimentally infected non-human primates, MV infects and depletes CD150+ memory lymphocytes. Based on this finding, we postulated the ‘immune amnesia’ model to explain the mechanism of measles immune suppression. A measles outbreak in the Dutch Orthodox Protestant community in 2013 provided a unique opportunity to test this hypothesis in unvaccinated children.

Materials and methods
We performed an observational cohort study and enrolled more than 100 unvaccinated children before or early after MV infection. To determine levels of virus shedding and phenotypes of MV-infected cells (Cohort A), nose and throat swabs and blood samples were collected from patients with clinical signs of prodromal measles. To determine whether lymphocyte populations were depleted after measles (Cohort B), we collected paired blood samples from healthy children before and after measles.

In Cohort A, we found that virus was shed more efficiently in the nose than in the throat. In the PBMC, we detected MV-infected memory CD4+ T, CD8+ T and B cells. In Cohort B, we found reduced frequencies of circulating memory B cells and increased frequencies of regulatory T and transitional B cells after measles.

Discussion and Conclusion
We show that measles viraemia in prodromal measles patients is largely mediated by MV-infected memory lymphocytes. Measles had a lasting impact on circulating lymphocyte subsets after recovery from the disease. These data support our immune amnesia hypothesis and offer an explanation for the previously observed long-term effects of measles on host resistance.
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