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Abstract
Antibodies constitute a critical component of the naturally acquired immunity that develops following frequent exposure to malaria. However, specific antibody titres have been reported to decline rapidly in the absence of reinfection, supporting the widely perceived notion that malaria infections fail to induce durable immunological memory responses. Currently, direct evidence for the presence or absence of immune memory to malaria is limited. In this study, we analysed the longevity of both antibody and B cell memory responses to malaria antigens among individuals who were living in an area of extremely low malaria transmission in northern Thailand, and who were known either to be malaria naïve or to have had a documented clinical attack of P. falciparum and/or P. vivax in the past 6 years. We found that exposure to malaria results in the generation of relatively avid antigen-specific antibodies and the establishment of populations of antigen-specific memory B cells in a significant proportion of malaria-exposed individuals. Both antibody and memory B cell responses to malaria antigens were stably maintained over time in the absence of reinfection. In a number of cases where antigen-specific antibodies were not detected in plasma, stable frequencies of antigen-specific memory B cells were nonetheless observed, suggesting that circulating memory B cells may be maintained independently of long-lived plasma cells. We conclude that infrequent malaria infections are capable of inducing long-lived antibody and memory B cell responses.
Highlights
Malaria, a parasitic disease of humans caused predominantly by two species of Plasmodium, P. falciparum and P. vivax, remains an important cause of mortality and morbidity in many parts of the world
We identified individuals living in an area of very low malaria endemicity in Northern Thailand who were either malaria naıve or who had had recorded clinical episodes of P. falciparum or P vivax infection some years previously and characterised the antibody and memory B cell response to a variety of discrete P. falciparum and P. vivax antigens under conditions of infrequent re-exposure/boosting of the immune response
Antibodies are critical in protection against blood stage malaria infection through numerous, diverse mechanisms [2,3]
Summary
A parasitic disease of humans caused predominantly by two species of Plasmodium, P. falciparum and P. vivax, remains an important cause of mortality and morbidity in many parts of the world. Development of a vaccine against malaria has proven challenging due to the complex nature of the parasite and to the difficulty in correlating naturally-acquired immune responses with clinical immunity. It is widely believed that periodic reinfection is required to maintain acquired immunity to malaria and that antimalarial antibodies are short-lived in the absence of reinfection (reviewed in [4]); implying that B cell memory to malaria may be defective or suboptimal. The development and persistence of B cell memory following malaria infection has long been a matter of debate (reviewed in [5]). Very few studies have examined the induction and maintenance of malaria-specific memory B cells in humans. Dorfman et al [14] were frequently unable to detect circulating malaria-specific B cells in antibody seropositive children, but it is unclear whether this reflects an absence of such cells or a lack of sensitivity in the assays used to Author Summary
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