Abstract
Dengue is endemic in tropical countries worldwide and the four dengue virus serotypes often co-circulate. Infection with one serotype results in high titers of cross-reactive antibodies produced by plasmablasts, protecting temporarily against all serotypes, but impairing protective immunity in subsequent infections. To understand the development of these plasmablasts, we analyzed virus-specific B cell properties in patients during acute disease and at convalescence. Plasmablasts were unrelated to classical memory cells expanding in the blood during early recovery. We propose that only a small subset of memory B cells is activated as plasmablasts during repeat infection and that plasmablast responses are not representative of the memory B cell repertoire after dengue infection.
Highlights
With 390 million people infected every year, dengue is a global concern [1]
Because we observed distinct non-overlapping repertoires in virusspecific plasmablasts and memory B cells (MBC) generated after dengue virus (DENV) infection, we investigated whether monoclonal antibodies derived from each of the two populations could be identified and discriminated based on their Ig heavy chain variable region (IgVH) sequences
It is less clear which B cells enter each path, and how the plasmablast and classical memory B cell population is related during acute stages of infection
Summary
With 390 million people infected every year, dengue is a global concern [1]. Over the past decades, the virus has spread from South East Asia to regions across the world with climates favorable for breeding of the transmitting vector, the Aedes or “tiger” mosquito. The dengue virus (DENV) complex comprises four antigenically related viruses (DENV-1 to 4) from the flavivirus family, and infection with one serotype generates both serotype-specific and cross-reactive antibodies [2]. During heterotypic re-infection, the antibody response is dominated by cross-reactive antibodies binding to regions in the viral proteins that are conserved across all serotypes [3,4]. At the same time, neutralizing antibodies against the serotype of the previous infection are often amplified more efficiently than antibodies against the new infecting serotype, which can result in increased disease severity when an individual is re-infected with a different serotype, a phenomenon previously described as original antigenic sin [5,6]
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