Abstract
Clinical immunity to malaria declines in the absence of repeated parasite exposure. However, little is known about how B cell populations and antigen-specific memory B cells change in the absence of P. falciparum infection. A successful indoor residual insecticide spraying campaign in a highland area of western Kenya, led to an absence of blood-stage P. falciparum infection between March 2007 and April 2008. We assessed memory B cell responses in 45 adults at the beginning (April 2008) and end (April 2009) of a subsequent 12-month period during which none of the adults had evidence of asymptomatic parasitemia or clinical disease. Antibodies and memory B cells to the 42-kDa portion of the merozoite surface protein-1 (MSP-142) were measured using ELISA and ELISPOT assays, respectively. B cell populations were characterized by flow cytometry. From 2008 to 2009, the prevalence of MSP-142-specific memory B cells (45% vs. 55%, respectively, P = 0.32) or antibodies (91% vs. 82%, respectively, P = 0.32) did not differ significantly, although specific individuals did change from positive to negative and vice versa, particularly for memory B cells, suggesting possible low-level undetected parasitemia may have occurred in some individuals. The magnitude of MSP-142-specific memory B cells and levels of antibodies to MSP-142 also did not differ from 2008 to 2009 (P>0.10 for both). However, from 2008 to 2009 the proportions of both class-switched atypical (CD19+IgD-CD27-CD21-IgM-) and class-switched activated (CD19+IgD-CD27+CD21-IgM-) memory B cells decreased (both P<0.001). In contrast, class-switched resting classical memory B cells (CD19+IgD-CD27+CD21+IgM-) increased (P<0.001). In this area of seasonal malaria transmission, a one- year absence of detectable P. falciparum infection was not associated with changes in the prevalence or level of MSP-142 specific memory B cells, but was associated with major changes in overall memory B cell subsets.
Highlights
Clinical immunity to Plasmodium falciparum malaria is acquired and maintained by repeated exposure to the parasite [1]
None of the 45 participants had an episode of clinical malaria during the one-year investigation period or in the preceding eight months, and all tested negative for P. falciparum by microscopy in repeated surveys for asymptomatic parasitemia before (July 2007 and November 2007) and during (April 2008, August 2008, October 2008, January 2009 and April, 2009) the twelve-month study period
We document that antibodies and memory B cell (MBC) to MSP142 are stable over a period of at least 12 months in the absence of detectable P. falciparum infection in previously malaria-exposed adults in a highland area of Kenya
Summary
Clinical immunity to Plasmodium falciparum malaria is acquired and maintained by repeated exposure to the parasite [1]. Repeated parasite exposure provides protection against severe disease in adults and older children in high transmission settings. This generally correlates with an age-related increase in antibody levels to blood stage Plasmodium vaccine-candidate antigens such as merozoite surface protein-1 (MSP-1) [3,4,5]. Studies in adults from Thailand and Madagascar done years after the most recent exposure to P. falciparum demonstrated the presence of long-lived memory B cell (MBC) populations and antibodies to P. falciparum antigens, including MSP-1 [8,9]. The dynamics of P. falciparum antigen-specific memory B cell responses over time and their alteration with changes in transmission intensity have not been studied to date
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call