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Plasmodium vivax is the predominant malaria parasite in Latin America. Its colonization history in the region is rich and complex, and is still highly debated, especially about its origin(s). Our study employed cutting-edge population genomic techniques to analyze whole genome variation from 620 P. vivax isolates, including 107 newly sequenced samples from West Africa, Middle East, and Latin America. This sampling represents nearly all potential source populations worldwide currently available. Analyses of the genetic structure, diversity, ancestry, coalescent-based inferences, including demographic scenario testing using Approximate Bayesian Computation, have revealed a more complex evolutionary history than previously envisioned. Indeed, our analyses suggest that the current American P. vivax populations predominantly stemmed from a now-extinct European lineage, with the potential contribution also from unsampled populations, most likely of West African origin. We also found evidence that P. vivax arrived in Latin America in multiple waves, initially during early European contact and later through post-colonial human migration waves in the late 19th-century. This study provides a fresh perspective on P. vivax's intricate evolutionary journey and brings insights into the possible contribution of West African P. vivax populations to the colonization history of Latin America. Author summary: Our study investigates the origins and spread of Plasmodium vivax in Latin America, the primary malaria parasite in this region. By analyzing genetic data from 620 P. vivax samples worldwide, including new samples from West Africa, the Middle East, and Latin America, we were able to reconstruct the evolutionary history of the parasite in this region. Our findings indicate that the current P. vivax strains in Latin America mainly descended from a now-extinct European lineage. Additionally, we found evidence suggesting that several migration waves following human migrations waves may have contributed to the parasite diversity, with possible contributions from West African populations during the transatlantic slave trade (16th to 19th century) and further input from Europe during post-colonial human migrations in the late 19th century. This study offers a fresh perspective on how historical human migrations have shaped the genetic landscape of P. vivax in Latin America. These insights are valuable for understanding the parasite evolution and may help inform strategies for malaria control and prevention in the future. [ABSTRACT FROM AUTHOR]

The protozoan Toxoplasma gondii is a ubiquitous and highly prevalent parasite that can theoretically infect all warm-blooded vertebrates. In humans, toxoplasmosis causes infections in both immunodeficient and immunocompetent patients, congenital toxoplasmosis, and ocular lesions. These manifestations have different degrees of severity. Clinical severity is determined by multiple factors, including the genotype of the T. gondii strain involved in the infection. T. gondii exhibits remarkable genetic diversity, which varies according to geography and ecotype (domestic or wild). Previous studies have demonstrated that wild strains of T. gondii are of particular epidemiological interest, as they have been associated with more severe forms of toxoplasmosis in different regions of the world. However, no data on wild strains of T. gondii are available from Africa. In this study, we describe for the first time a wild T. gondii strain from Africa. Wild animals from the forest environment of Gabon, Central Africa, were screened for chronic infection with T. gondii using quantitative PCR. The infecting T. gondii strains were genotyped whenever possible by the analysis of 15 microsatellite markers and by whole-genome sequencing. A new T. gondii genotype was identified in the DNA extract from a heart sample of a duiker (Cephalophus sp.) and was found to be highly divergent from previously described T. gondii populations worldwide, including those from domestic environments in Gabon. This discovery suggests the existence of a wild T. gondii population in Africa. The role of wild T. gondii strains in the incidence of severe toxoplasmosis in Africa remains unclear and requires further investigation. Author summary: The emergence of new pathogens from wildlife is today a well-recognized health threat. Studying these infectious agents has proven to be challenging due to the difficulty in accessing samples from wild animals. In the present study, we took advantage of a recent survey on the viral carriage of wild animals from Gabon, Central Africa, to screen animal samples for the presence of the zoonotic protozoan Toxoplasma gondii. This ubiquitous and highly prevalent parasite can theoretically infect all warm-blooded vertebrates, including humans. This parasite is the etiological agent of toxoplasmosis, a disease causing a substantial public health burden worldwide through different clinical manifestations and varying degrees of severity. A novel genotype was identified in a wild antelope from the Gabonese forest, and was found to be highly divergent from previously described T. gondii populations worldwide, including those from the domestic environment in Gabon. This discovery suggests the existence of a wild T. gondii population in Africa. It has been shown that wild strains of T. gondii are of significant epidemiological relevance, as they have been associated with more severe forms of toxoplasmosis in different regions of the world. The implications of wild T. gondii strains in the incidence of severe toxoplasmosis in Africa remain unclear and merit further investigation. [ABSTRACT FROM AUTHOR]

Pathogens, which have recently colonized a new host species or new populations of the same host, are interesting models for understanding how populations may evolve in response to novel environments. During its colonization of South America from Africa, Plasmodium falciparum, the main agent of malaria, has been exposed to new conditions in distinctive new human populations (Amerindian and populations of mixed origins) that likely exerted new selective pressures on the parasite's genome. Among the genes that might have experienced strong selective pressures in response to these environmental changes, the eba genes (erythrocyte-binding antigens genes), which are involved in the invasion of the human red blood cells, constitute good candidates. In this study, we analysed, in South America, the polymorphism of three eba genes (eba-140, eba-175, eba-181) and compared it to the polymorphism observed in African populations. The aim was to determine whether these genes faced selective pressures in South America distinct from what they experienced in Africa. Patterns of genetic variability of these genes were compared to the patterns observed at two housekeeping genes (adsl and serca) and 272 SNPs to separate adaptive effects from demographic effects. We show that, conversely to Africa, eba-140 seemed to be under stronger diversifying selection in South America than eba-175. In contrast, eba-181 did not show any sign of departure from neutrality. These changes in the patterns of selection on the eba genes could be the consequence of changes in the host immune response, the host receptor polymorphisms and/or the ability of the parasite to silence or express differentially its invasion proteins.

Plasmodium vivax is considered to be absent from Central and West Africa because of the protective effect of Duffy negativity. However, there are reports of persons returning from these areas infected with this parasite and observations suggesting the existence of transmission. Among the possible explanations for this apparent paradox, the existence of a zoonotic reservoir has been proposed. May great apes be this reservoir? We analyze the mitochondrial and nuclear genetic diversity of P. vivax parasites isolated from great apes in Africa and compare it to parasites isolated from travelers returning from these regions of Africa, as well as to human isolates distributed all over the world. We show that the P. vivax sequences from parasites of great apes form a clade genetically distinct from the parasites circulating in humans. We show that this clade's parasites can be infectious to humans by describing the case of a traveler returning from the Central African Republic infected with one of them. The relationship between this P. vivax clade in great apes and the human isolates is discussed.

The origin of Plasmodium falciparum in South America is controversial. Some studies suggest a recent introduction during the European colonizations and the transatlantic slave trade. Other evidence--archeological and genetic--suggests a much older origin. We collected and analyzed P. falciparum isolates from different regions of the world, encompassing the distribution range of the parasite, including populations from sub-Saharan Africa, the Middle East, Southeast Asia, and South America. Analyses of microsatellite and SNP polymorphisms show that the populations of P. falciparum in South America are subdivided in two main genetic clusters (northern and southern). Phylogenetic analyses, as well as Approximate Bayesian Computation methods suggest independent introductions of the two clusters from African sources. Our estimates of divergence time between the South American populations and their likely sources favor a likely introduction from Africa during the transatlantic slave trade.

Recent molecular exploration of the Plasmodium species circulating in great apes in Africa has revealed the existence of a large and previously unknown diversity of Plasmodium. For instance, gorillas were found to be infected by parasites closely related to Plasmodium falciparum, suggesting that the human malignant malaria agent may have arisen after a transfer from gorillas. Although this scenario is likely in light of the data collected in great apes, it remained to be ascertained whether P. falciparum-related parasites may infect other nonhuman primates in Africa. Using molecular tools, we here explore the diversity of Plasmodium species infecting monkeys in Central Africa. In addition to previously described Hepatocystis and Plasmodium species (Plasmodium gonderi and Plasmodium sp DAJ-2004), we have found one African monkey to be infected by a P. falciparum-related parasite. Examination of the nuclear and mitochondrial genomes of this parasite reveals that it is specific of nonhuman primates, indicating that P. falciparum-related pathogens can naturally circulate in some monkey populations in Africa. We also show that at least two distinct genetic entities of P. falciparum infect nonhuman primates and humans, respectively. Our discoveries bring into question the proposed gorilla origin of human P. falciparum.

Until very recently, only one species (P. reichenowi) was known to be a phylogenetic sister lineage of P. falciparum, the main malignant agent of human malaria. In 2009 and 2010, new studies have revealed the existence of several new phylogenetic species related to this deadly parasite and infecting chimpanzees and gorillas in Africa. These discoveries invite us to explore a whole set of new questions, which we briefly do in this article.

Plasmodium reichenowi, a chimpanzee parasite, was until very recently the only known close relative of Plasmodium falciparum, the most virulent agent of human malaria. Recently, Plasmodium gaboni, another closely related chimpanzee parasite, was discovered, suggesting that the diversity of Plasmodium circulating in great apes in Africa might have been underestimated. It was also recently shown that P. reichenowi is a geographically widespread and genetically diverse chimpanzee parasite and that the world diversity of P. falciparum is fully included within the much broader genetic diversity of P. reichenowi. The evidence indicates that all extant populations of P. falciparum originated from P. reichenowi, likely by a single transfer from chimpanzees. In this work, we have studied the diversity of Plasmodium species infecting chimpanzees and gorillas in Central Africa (Cameroon and Gabon) from both wild-living and captive animals. The studies in wild apes used noninvasive sampling methods. We confirm the presence of P. reichenowi and P. gaboni in wild chimpanzees. Moreover, our results reveal the existence of an unexpected genetic diversity of Plasmodium lineages circulating in gorillas. We show that gorillas are naturally infected by two related lineages of parasites that have not been described previously, herein referred to as Plasmodium GorA and P. GorB, but also by P. falciparum, a species previously considered as strictly human specific. The continuously increasing contacts between humans and primate populations raise concerns about further reciprocal host transfers of these pathogens.