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Trop Med Int Health. 2007 Mar;12(3):431-44.

Associations between specific antibody responses and resistance to reinfection in a Senegalese population recently exposed to Schistosoma mansoni.

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1
Prince Leopold Institute of Tropical Medicine, Antwerp, Belgium.

Abstract

We examined associations between schistosome-specific antibody responses and reinfection in Senegalese individuals recently exposed to Schistosoma mansoni. The effects of treatment, age, intensity of infection and duration of exposure on schistosome-specific antibody responses were also investigated by comparing immune responses in individuals exposed for less than 3 years with responses in people exposed for more than 8 years. All individuals were bled before treatment as well as 6 and 12 weeks after. We used a statistical model that included interaction terms between time, age, infection intensity and duration of exposure. The overall patterns of most specific antibody responses by age were similar to those previously published for S. mansoni, Schistosoma japonicum and Schistosoma haematobium infections in different endemic areas. In general, a boost in specific antibody responses against adult worm antigen (SWA) was observed at 6 weeks after treatment whereas the majority of isotype responses against egg antigen (SEA) were not affected by treatment. Our analysis showed that the effect of treatment on schistosome-specific antibody responses is influenced by age, infection intensity and duration of exposure. We found no evidence that treatment matures the specific antibody response of children recently infected with S. mansoni. Our results indicate that the build-up of potentially protective immunoglobulin E (IgE) responses was associated with duration of exposure, or, in other words, experience of infection. Interestingly, in recently exposed individuals there was a significant association between IgA responses to SWA and resistance to reinfection. Resistance to reinfection and production of IgA-SWA was associated with adulthood independently of exposure patterns, suggesting that susceptibility to S. mansoni and the development of protective immune responses is age-dependent.

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