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. 2013 May;81(5):1585–1595. doi: 10.1128/IAI.01117-12

Fig 8.

Fig 8

Inhibition of erythrocyte binding to P. vivax MSP1P-19 expressed on COS-7 cells by naturally acquired antibodies and mouse anti-PvMSP1P-19 antibody. (A) COS-7 cells were transfected with pEGFP-HSVgD1_DBPII plasmid DNA expressing a GFP-DBPII fusion protein. Cells were subsequently incubated with anti-PvDBPII immune mouse sera at various dilutions before the addition of human erythrocytes. Binding was scored by counting the number of rosettes bound to COS-7 cells in 30 microscope fields (×200). Mouse antiserum against PBS as nonimmunized control (NI) and anti-Pvs25 (no erythrocyte-binding activity) immune mouse sera diluted 1:10 were included as negative controls (Pvs25). (B) Inhibition of erythrocyte binding to PvMSP1P-19 expressed on COS-7 cells by PvMSP1P immune mouse sera. Cells were then incubated with PvMSP1P immune mouse sera at various dilutions before the addition of human erythrocytes. (C) Inhibition of erythrocyte binding to PvMSP1P-19 expressed on COS-7 cells by vivax immune human sera. Cells were incubated with various dilutions of pooled sera from vivax malaria patients of ROK (ROK+) before the addition of human erythrocytes. Erythrocyte-binding activity was scored by counting the number of rosettes in 30 fields at a magnification of ×200. The percent binding was determined relative to a 1:10 dilution of pooled sera from areas of nonendemicity of ROK (ROK) as a negative control. Cells were incubated with various dilutions of the high-responding (high ROK+) (D) and low-responding (low ROK+) (E) vivax malaria sera before the addition of human erythrocytes. Error bars represent ± standard deviations.