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1.
Pathogens ; 11(9)2022 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-36145424

RESUMO

Human African Trypanosomiasis (HAT) is an infectious disease caused by protozoan parasites belonging to the Trypanosoma genus. In sub-Saharan Africa, there is a significant threat as many people are at risk of infection. Despite this, HAT is classified as a neglected tropical disease. Over the last few years, several studies have reported the existence of a wide diversity of trypanosome species circulating in African animals. Thus, domestic and wild animals could be reservoirs of potentially dangerous trypanosomes for human populations. However, very little is known about the role of domestic animals in maintaining the transmission cycle of human trypanosomes in central Africa, especially in Gabon, where serious cases of infection are recorded each year, sometimes leading to hospitalization or death of patients. Komo-Mondah, located within Estuaries (Gabonese province), stays the most active HAT disease focus in Gabon, with a mean of 20 cases per year. In this study, we evaluated the diversity and prevalence of trypanosomes circulating in domestic animals using the Polymerase Chain Reaction (PCR) technique. We found that 19.34% (53/274) of the domestic animals we studied were infected with trypanosomes. The infection rates varied among taxa, with 23.21% (13/56) of dogs, 16.10% (19/118) of goats, and 21.00% (21/100) of sheep infected. In addition, we have observed a global mixed rate of infections of 20.75% (11/53) among infected individuals. Molecular analyses revealed that at least six Trypanosome species circulate in domestic animals in Gabon (T. congolense, T. simiae, T. simiae Tsavo, T. theileri, T. vivax, T. brucei (including T. brucei brucei, and T. brucei gambiense)). In conclusion, our study showed that domestic animals constitute important potential reservoirs for trypanosome parasites, including T. brucei gambiense, which is responsible for HAT.

2.
PLoS Biol ; 16(8): e2006035, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-30142149

RESUMO

Although Plasmodium vivax is responsible for the majority of malaria infections outside Africa, little is known about its evolution and pathway to humans. Its closest genetic relative, P. vivax-like, was discovered in African great apes and is hypothesized to have given rise to P. vivax in humans. To unravel the evolutionary history and adaptation of P. vivax to different host environments, we generated using long- and short-read sequence technologies 2 new P. vivax-like reference genomes and 9 additional P. vivax-like genotypes. Analyses show that the genomes of P. vivax and P. vivax-like are highly similar and colinear within the core regions. Phylogenetic analyses clearly show that P. vivax-like parasites form a genetically distinct clade from P. vivax. Concerning the relative divergence dating, we show that the evolution of P. vivax in humans did not occur at the same time as the other agents of human malaria, thus suggesting that the transfer of Plasmodium parasites to humans happened several times independently over the history of the Homo genus. We further identify several key genes that exhibit signatures of positive selection exclusively in the human P. vivax parasites. Two of these genes have been identified to also be under positive selection in the other main human malaria agent, P. falciparum, thus suggesting their key role in the evolution of the ability of these parasites to infect humans or their anthropophilic vectors. Finally, we demonstrate that some gene families important for red blood cell (RBC) invasion (a key step of the life cycle of these parasites) have undergone lineage-specific evolution in the human parasite (e.g., reticulocyte-binding proteins [RBPs]).


Assuntos
Plasmodium vivax/genética , Plasmodium/genética , Animais , Sequência de Bases/genética , Culicidae , Eritrócitos/parasitologia , Evolução Molecular , Genoma/genética , Humanos , Malária/parasitologia , Malária Falciparum/parasitologia , Malária Vivax/genética , Pan troglodytes/genética , Filogenia , Plasmodium falciparum/genética
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