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- W52565503 abstract "Abstract Original antigenic sin is a phenomenon in which exposure to a novel influenza virus strain leads to production of antibodies against a related viral strain encountered in the past. These cross-reactive antibodies are produced at the expense of antibodies against novel epitopes in the current strain. The existence of original antigenic sin has been demonstrated in humans as well as mice, rabbits, guinea pigs and ferrets. Despite the fact that this phenomenon was first described in 1953, the mechanisms involved are poorly understood. We hypothesize that original antigenic sin results from selective activation of B cells, particularly memory B cells specific for cross-reactive antigenic determinants. The hemagglutinin of influenza viruses can bind to all B cells, irrespective of their B cell receptor specificity, via sialic acid binding. Such binding may activate memory B cells better because they have lower activation thresholds than naïve B cells. To test whether original antigenic sin resulted from targeting of the virus to B cells and activation of pre-existing memory B cells specific for influenza strains encountered in the past, we generated influenza viruses whose ability to bind to sialic acid receptors on B cell surfaces is severely diminished. Our results suggest such diminished B cell targeting modulates the induction of original antigenic sin." @default.
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- W52565503 date "2010-04-01" @default.
- W52565503 modified "2023-10-16" @default.
- W52565503 title "Altering hemagglutinin binding to B cells modulates original antigenic sin responses to influenza viruses (92.23)" @default.
- W52565503 doi "https://doi.org/10.4049/jimmunol.184.supp.92.23" @default.
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