negative individuals whose erythrocytes do not express the receptor are believed to be resistant to merozoite invasion although P. vivax infection has been reported in Duffy negative children in Kenya, suggesting a role in resistance to disease, not infection. This antigen may also play a role in erythrocyte invasion in the rodent malarial parasite P. yoelii. The epitope Fy6 is required for P. vivax invasion. The protection to P. vivax malaria conferred by the absence of the Duffy antigen appears to be very limited at best in Madagascar. Although 72% of the population are Duffy antigen negative, 8.8% of the Duffy antigen negative individuals were asymptomatic carriers of P. vivax. Malaria has also been found in Angola and Equatorial Guinea in Duffy negative individuals. P. vivax malaria in a Duffy antigen negative individual in Mauritania has also been reported. Similar infections have been reported in Brazil and Kenya. Additional cases of infection in Duffy antigen negative individuals have been reported from the Congo and Uganda. A study in Brazil of the protection against P. vivax offered by the lack of the Duffy antigen found no differential resistance to malaria vivax between Duffy antigen positive and negative individuals. Nancy Ma's night monkey (A. nancymaae) is used as an animal model of P. vivax infection. This species' erythrocytes possess the Duffy antigen and this antigen is used as the receptor for P. vivax on the erythrocytes in this species. Examination of this gene in 497 patients in the Amazonas State, Brazil, made by the doctor Sérgio Albuquerque, suggests that the genotypes FY*A/FY*B-33 and FY*B/FY*B-33 (where -33 refers to the null mutation at position -33 in the GATA box) may have an advantage over the genotypes FY*A/FY*B and FY*A/FY*A, FY*A/FY*B, FY*A/FY*X and FY*B/FY*X. FY*A/FY*B and FY*A/FY*A genotypes showed to be associated with increased rates of P. vivax infection and FY*B/FY*X and FY*A/FY*X were shown to be associated with the low levels of parasitism. A difference between the susceptibility to Plasmodium vivax malaria has been reported. Erythrocytes expressing Fya had 41-50% lower binding of P. vivax compared with Fyb cells. Individuals with the Fy(a+b-) phenotype have a 30-80% reduced risk of clinical vivax but not falciparum malaria. The binding of platelet factor 4 (CXCL4) appears to be critical for the platelet induced killing of P. falciparum. The Duffy antigen binding protein in P. vivax'' is composed of three subdomains and is thought to function