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. 2009 Oct 1;200(7):1166-75.
doi: 10.1086/605652.

Transmission-dependent tolerance to multiclonal Plasmodium falciparum infection

Anna Färnert  1 , Thomas N Williams, Tabitha W Mwangi, Anna Ehlin, Greg Fegan, Alex Macharia, Brett S Lowe, Scott M Montgomery, Kevin Marsh
Affiliations

Transmission-dependent tolerance to multiclonal Plasmodium falciparum infection

Anna Färnert et al. J Infect Dis. .

Abstract

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.

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Figures

Figure 1
Figure 1
Number of asymptomatic children 0-10 years old infected with different numbers of msp2 genotypes in a cross-sectional survey conducted in Ngerenya, which has a low level of transmission (n = 273), and in Chonyi, which has a moderate level of transmission (n = 264).
Figure 2
Figure 2
Mean number of msp2 genotypes in the children positive by polymerase chain reaction in Ngerenya and Chonyi, by the 2 respective allelic types FC27 and IC.
Figure 3
Figure 3
Kaplan-Meier estimates of the time to the last episode of malaria and treatment before the survey (A) and the time to the first subsequent episode of malaria (fever and >2500 Plasmodium falciparum parasites/μL) after the survey in asymptomatic children infected with different numbers of msp2 genotypes (adjusted for age and parasite density).
Figure 4
Figure 4
Prospective risk of malaria in relation to the number of clones in asymptomatic children in 2 areas of low and moderate transmission in Kilifi, Kenya (present study), and in an area of high transmission in Rufiji, Tanzania [16]. The risk is assessed by Cox regression as the time to the first malaria episode after the survey. The hazard ratios (HRs) are adjusted for age and parasite density.
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