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. 2015 Dec 9;23(2):117-24.
doi: 10.1128/CVI.00501-15. Print 2016 Feb.

Acquisition and Longevity of Antibodies to Plasmodium vivax Preerythrocytic Antigens in Western Thailand

Affiliations

Acquisition and Longevity of Antibodies to Plasmodium vivax Preerythrocytic Antigens in Western Thailand

Rhea J Longley et al. Clin Vaccine Immunol. .

Abstract

Plasmodium vivax is now the dominant Plasmodium species causing malaria in Thailand, yet little is known about naturally acquired immune responses to this parasite in this low-transmission region. The preerythrocytic stage of the P. vivax life cycle is considered an excellent target for a malaria vaccine, and in this study, we assessed the stability of the seropositivity and the magnitude of IgG responses to three different preerythrocytic P. vivax proteins in two groups of adults from a region of western Thailand where malaria is endemic. These individuals were enrolled in a yearlong cohort study, which comprised one group that remained P. vivax free (by quantitative PCR [qPCR] detection, n = 31) and another that experienced two or more blood-stage P. vivax infections during the year of follow up (n = 31). Despite overall low levels of seropositivity, IgG positivity and magnitude were long-lived over the 1-year period in the absence of qPCR-detectable blood-stage P. vivax infections. In contrast, in the adults with two or more P. vivax infections during the year, IgG positivity was maintained, but the magnitude of the response to P. vivax circumsporozoite protein 210 (CSP210) decreased over time. These findings demonstrate that long-term humoral immunity can develop in low-transmission regions.

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Figures

FIG 1
FIG 1
IgG magnitude and the effect of current blood-stage P. vivax infections. IgG responses to P. vivax (A) CSP247, (B) CSP210, and (C) CelTOS at visit 1. Volunteers are stratified into those uninfected throughout the cohort (group 1), those exposed but currently uninfected (group 2), and those exposed but currently infected (group 3). The dashed lines represent protein-specific positivity cutoffs. Statistical differences between the three groups were assessed using the Kruskal-Wallis test with Dunn's multiple-comparison test. *, P < 0.05.
FIG 2
FIG 2
Magnitude of the IgG response and exposure to P. vivax infection. IgG responses to P. vivax proteins at visits 1 and 14 were stratified by the 31 adults who experienced no P. vivax infections (uninfected) and by the 31 adults who experienced 2 or more qPCR-detectable blood-stage P. vivax infections (exposed) during the 1-year cohort. Individual data points and the median are shown. The dashed lines represent protein-specific positivity cutoffs. Statistical difference between uninfected and exposed adults over the two time points was assessed using a two-way ANOVA: (A) P = 0.019, (B) P = 0.0047, and (C) P = 0.5.
FIG 3
FIG 3
Longevity of the IgG magnitude in uninfected volunteers. IgG responses to P. vivax (A) CSP247 and (B) CSP210 in the 31 uninfected volunteers were stratified by visits 1 and 14. The left panels show individual data points and the median, while the right panels show the individual change over time for individuals who were seropositive. The dashed lines represent protein-specific positivity cutoffs. Statistical difference over visits was assessed using the Wilcoxon matched-pairs signed-rank test: (A) P = 0.26, and (B) P = 0.46.
FIG 4
FIG 4
Longevity of the IgG magnitude in exposed volunteers. IgG responses to P. vivax (A) CSP247, (B) CSP210, and (C) CelTOS in the 31 exposed volunteers were stratified by visits 1 and 14. The left panels show individual data points and the median, while the right panels show the individual change over time for individuals who were seropositive. The dashed lines represent protein-specific positivity cutoffs. Statistical difference over visits was assessed using the Wilcoxon matched-pairs signed-rank test: (A) P > 0.99, (B) P = 0.0014, and (C) P = 0.77.

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