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dc.contributor.authorFärnert, Anna
dc.contributor.authorWilliams, Thomas N.
dc.contributor.authorMwangi, Tabitha W.
dc.contributor.authorEhlin, Anna
dc.contributor.authorFegan, Greg
dc.contributor.authorMacharia, Alex
dc.contributor.authorLowe, Brett S.
dc.contributor.authorMontgomery, Scott M.
dc.contributor.authorMarsh, Kevin
dc.date.accessioned2013-10-30T15:42:12Z
dc.date.available2013-10-30T15:42:12Z
dc.date.issued2009-10-01
dc.identifier.otherdoi:10.1086/605652
dc.identifier.urihttp://hdl.handle.net/123456789/571
dc.descriptionEurope PMC Funders Group Author Manuscript J Infect Dis. Author manuscript; available in PMC 2010 April 01.en_US
dc.description.abstractAbstract Whether the number of concurrent clones in asymptomatic Plasmodium falciparum infections reflects the degree of host protection was investigated in children living in areas with different levels of transmission on the coast of Kenya. The number of concurrent clones was determined on the basis of polymorphism in msp2, which encodes the vaccine candidate antigen merozoite surface protein 2. In a low-transmission area, most children had monoclonal infections, and diversity did not predict a risk of clinical malaria. In an area of moderate transmission, asymptomatic infections with 2 clones were, compared with 1 clone, associated with an increased risk of subsequent malaria. In a comparative assessment in a high-transmission area in Tanzania, multiclonal infections conferred a reduced risk. The different nonlinear associations between the number of clones and malaria morbidity suggest that levels of tolerance to multiclonal infections are transmission dependent as a result of cumulative exposure to antigenically diverse P. falciparum infections.en_US
dc.language.isoenen_US
dc.publisherJournal of Infectious Diseasesen_US
dc.titleTransmission-Dependent Tolerance to Multiclonal Plasmodium falciparum Infectionen_US
dc.typeArticleen_US


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