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It is generally accepted that it originated in humans as a consequence of host capture from macaques to hominids in Southeast Asia [17,18]. Interestingly, despite numerous studies on Plasmodium parasites infecting Southeast Asian primates (including the orangutan, the Asian great ape), none of them was found to be infected with P.?vivax [19]. On the other hand, captive and wild-living African gorillas and chimpanzees were recently found to be infected with a Plasmodium parasite with mitochondrial DNA similar to that of human P.?vivax [7,20,21]. In 2003, Carter argued that ��P.vivax would have been isolated in human African populations during the Alectinib datasheet late ice age between 100?000 and 20?000?years ago�� [22]. If this is the case, the P.?vivax population currently observed in great apes could be the descendants of this ancient P.?vivax lineage, which led to red blood cell (RBC) Duffy-negative selection in African human populations. Thus, the P.?vivax cases described in non-African people returning from Africa might result from zoonotic ape transmission [23]. However, serological studies have demonstrated an immune response specific to P.?vivax in West Central African populations, and molecular diagnosis evidence has confirmed the possibility of such infections in Duffy antigen-negative humans [24�C26]. This strongly suggests that P.?vivax exploits an alternative pathway to invade Duffy-negative RBCs. This stresses the need to determine the epidemiology of P.?vivax throughout Africa and evaluate the capacity of new Duffy-independent P.?vivax strains to emerge. Comparative Tryptophan synthase surveys need to be performed in ape populations to evaluate their possible involvement in the emergence and spread of P.?vivax in Africa. Plasmodium knowlesi, transmitted by the Anopheles leucosphyrus group, is a parasite that naturally infects primates belonging to the genus Macaca in Southeast Asia [1]. For the past 10?years, the increasing systematic use of relevant molecular malaria diagnosis has highlighted an impressive number of unsuspected human P.?knowlesi infections. The first cases were detected in Malaysia and the Philippines [27,28]. Today, P.?knowlesi is found infecting Thai, Vietnamese and Cambodian populations, for whom environmental anthropization overlaps with the natural /www.selleckchem.com/PI3K.html geographical distribution of macaques [29�C31]. Modifications of the wildlife population biogeography might favour close interactions and parasite exchanges. The question remains: is P.?knowlesi spreading over Southeast Asia via interhuman exchanges as a new human outbreak, or only via macaques to human host switches? Furthermore, have these new human P.?knowlesi infections originated recently, or are they simply more readily detected by molecular tools [32�C34]? In Cambodia, it seems that the presence of this species in the human population is recent, and no macaques have yet been found to be infected with P.?knowlesi [31]. This could argue for possible interhuman transmission. Considering that P.