The 243 individuals experienced a total of 266 clinical malaria attacks (mean = 1.09, 95%CI: 0.88-1.30). The number of clinical malaria attacks experienced per individual varied from 0 (140 individuals) to 7 (1 individual). Recordings of the entomological inoculation rate indicated a mean of 170 infected bites/person during this time period. Twenty-nine percent of the seronegative individuals (with check details no detected anti-MSP1 block2 antibodies) experienced a clinical attack during that period, P505-15 mw compared

with 15% of individuals with anti-block2 antibodies. Using a Poisson regression model, the crude estimates of the Incidence Rate Ratio (IRR) of malaria attacks associated with the presence of antibodies to one allelic family Silmitasertib mouse or ≥ 2 families (no antibodies as reference group) were 0.55 (95%CI: 0.38-0.80) and 0.21 (95%CI: 0.08-0.58),

respectively (P < 0.0001). In a multivariate Poisson regression analysis, this association was independent of haemoglobin type or ethnic group. However, it was confounded by age, i.e. within the age groups, there was no significant association between the incidence of clinical malaria attacks and the number of MSP1 block2 allelic families recognized. Analysis of the response during a high transmission season To study the impact of novel infections during the transmission season on the humoral response to MSP1 block2, we investigated the fingerprick blood samples collected from 25 seropositive individuals throughout the high transmission season. By the end of December 1998, namely five months after the cross-sectional sampling, the anti-MSP1 block2 antibody level was reduced by ≥ 2-fold in 15 subjects (59%), had varied less than 2-fold in 9 individuals (36%) (typical profiles are shown in Figure 8 upper and middle panel, respectively) and was ≥ 2-fold higher in one

individual (Figure 8, lower panel). Importantly, when a Baf-A1 nmr change was observed, it concerned the intensity of the reaction but not its specificity. In other words, responding individuals usually reacted with the same pool(s) and within the pool(s) with the same individual peptide(s) before and after the transmission season. In none of the studied individuals were novel antibody specificities stably acquired during that time period, despite an elevated infection rate. Figure 8 Typical profiles of the temporal evolution of MSP1 block2- specific IgG before and after the 1998 rainy season. Antibodies were assayed from 25 individuals in August 1998 (yellow) and December 1998, i.e. after a rainy season when each inhabitant was exposed to a mean of 170 infected bites. Anti-MSP1 block2 specific IgG was assessed by ELISA on 16 pools of biotinylated peptides.