In the case of viruses, such as hepatitis C virus (HCV) or human immunodeficiency virus (HIV), there are studies showing either monoclonal or polyclonal antibodies can interfere with the effects of other monoclonal or polyclonal antibodies in a neutralizing assay [31] [32] [33] [34] [35] . In these studies, the antibodies recognize different epitopes on the same antigen and the mechanism of the interference may be explained by steric blocking [36] and/or conformational rearrangement induced by the non-neutralizing antibody. A similar phenomenon has been reported with the P. falciparum Merozoite Surface Protein 1 (MSP1), another bloodstage vaccine candidate. In the case of MSP1, a proportion of anti-MSP1 antibodies called ''blocking'' antibodies, which are found in people living in malaria endemic areas, competes with an anti-MSP1 monoclonal antibody capable of inhibiting merozoite invasion of erythrocytes in vitro, as judged by a competition ELISA and by an MSP1 processing assay [37] [38] [39] . However, it is not clear whether such ''blocking'' antibodies interfere with the activity of anti-MSP1 antibody, especially the activity of polyclonal antibodies, in a biological assay, such as GIA. It has been reported that human ''blocking'' antibodies interfere with the invasioninhibitory activity of mouse anti-MSP1 monoclonal antibody (mAb) 12.8, but the same human antibodies did not block the biological activity of another inhibitory mAb 12.10 [37] . To our knowledge, non-AMA1 IgG is the only reported antibodies which have been shown to interfere with the growth-inhibitory activity induced by human antigen-specific polyclonal antibodies. However, it is conceivable that similar functional interference effect exists in antibodies against other malarial antigens, including MSP1.