TY - JOUR

T1 - Malaria-induced acquisition of antibodies to Plasmodium falciparum variant surface antigens

AU - Ofori, Michael F

AU - Dodoo, Daniel

AU - Staalsoe, Trine

AU - Kurtzhals, Jørgen

AU - Koram, Kwadwo

AU - Theander, Thor G

AU - Akanmori, Bartholomew D

AU - Hviid, Lars

N1 - Keywords: Aging; Animals; Antibodies, Protozoan; Antibody Specificity; Antigens, Protozoan; Antigens, Surface; Child; Child, Preschool; Genotype; Ghana; Humans; Infant; Longitudinal Studies; Malaria, Falciparum; Plasmodium falciparum; Population Surveillance; Seasons

PY - 2002

Y1 - 2002

N2 - In areas of intense Plasmodium falciparum transmission, protective immunity is acquired during childhood in parallel with acquisition of agglutinating antibodies to parasite-encoded variant surface antigens (VSA) expressed on parasitized red blood cells. In a semi-immune child in such an area, clinical disease is caused mainly by parasites expressing VSA not recognized by preexisting VSA-specific antibodies in that child. Such malaria episodes are known to cause an increase in agglutinating antibodies specifically recognizing VSA expressed by the parasite isolate causing the illness, whereas antibody responses to other parasite isolates are relatively unaffected. However, the detailed kinetics of this VSA antibody acquisition are unknown and hence were the aim of this study. We show that P. falciparum malaria in Ghanaian children generally caused a rapid and sustained increase in variant-specific VSA antibody levels, while more transient and limited increases in levels of antibodies to VSA expressed by other parasite isolates were also seen. Plasma VSA antibody levels were positively correlated with the age of the healthy plasma donors but negatively correlated with the age of the parasite donors (the malaria patient). The data from this first detailed longitudinal study of acquisition of VSA antibodies support the hypothesis that naturally acquired protective immunity to P. falciparum malaria is mediated, at least in part, by VSA-specific antibodies.

AB - In areas of intense Plasmodium falciparum transmission, protective immunity is acquired during childhood in parallel with acquisition of agglutinating antibodies to parasite-encoded variant surface antigens (VSA) expressed on parasitized red blood cells. In a semi-immune child in such an area, clinical disease is caused mainly by parasites expressing VSA not recognized by preexisting VSA-specific antibodies in that child. Such malaria episodes are known to cause an increase in agglutinating antibodies specifically recognizing VSA expressed by the parasite isolate causing the illness, whereas antibody responses to other parasite isolates are relatively unaffected. However, the detailed kinetics of this VSA antibody acquisition are unknown and hence were the aim of this study. We show that P. falciparum malaria in Ghanaian children generally caused a rapid and sustained increase in variant-specific VSA antibody levels, while more transient and limited increases in levels of antibodies to VSA expressed by other parasite isolates were also seen. Plasma VSA antibody levels were positively correlated with the age of the healthy plasma donors but negatively correlated with the age of the parasite donors (the malaria patient). The data from this first detailed longitudinal study of acquisition of VSA antibodies support the hypothesis that naturally acquired protective immunity to P. falciparum malaria is mediated, at least in part, by VSA-specific antibodies.

U2 - 10.1128/IAI.70.6.2982-2988.2002

DO - 10.1128/IAI.70.6.2982-2988.2002

M3 - Journal article

C2 - 12010988

VL - 70

SP - 2982

EP - 2988

JO - Infection and Immunity

JF - Infection and Immunity

SN - 0019-9567

IS - 6

ER -