The genome of the zoonotic malaria parasite Plasmodium simium reveals adaptations to host switching
2021
Tobias Mourier | Denise Anete Madureira de Alvarenga | Abhinav Kaushik | Anielle de Pina-Costa | Olga Douvropoulou | Qingtian Guan | Francisco J. Guzmán-Vega | Sarah Forrester | Filipe Vieira Santos de Abreu | Cesare Bianco Júnior | Julio Cesar de Souza Junior | Silvia Bahadian Moreira | Zelinda Maria Braga Hirano | Alcides Pissinatti | Maria de Fátima Ferreira-da-Cruz | Ricardo Lourenço de Oliveira | Stefan T. Arold | Daniel C. Jeffares | Patrícia Brasil | Cristiana Ferreira Alves de Brito | Richard Culleton | Cláudio Tadeu Daniel-Ribeiro | Arnab Pain
Abstract Background Plasmodium simium, a malaria parasite of non-human primates (NHP), was recently shown to cause zoonotic infections in humans in Brazil. We sequenced the P. simium genome to investigate its evolutionary history and to identify any genetic adaptions that may underlie the ability of this parasite to switch between host species. Results Phylogenetic analyses based on whole genome sequences of P. simium from humans and NHPs reveals that P. simium is monophyletic within the broader diversity of South American Plasmodium vivax, suggesting P. simium first infected NHPs as a result of a host switch of P. vivax from humans. The P. simium isolates show the closest relationship to Mexican P. vivax isolates. Analysis of erythrocyte invasion genes reveals differences between P. vivax and P. simium, including large deletions in the Duffy-binding protein 1 (DBP1) and reticulocyte-binding protein 2a genes of P. simium. Analysis of P. simium isolated from NHPs and humans revealed a deletion of 38 amino acids in DBP1 present in all human-derived isolates, whereas NHP isolates were multi-allelic. Conclusions Analysis of the P. simium genome confirmed a close phylogenetic relationship between P. simium and P. vivax, and suggests a very recent American origin for P. simium. The presence of the DBP1 deletion in all human-derived isolates tested suggests that this deletion, in combination with other genetic changes in P. simium, may facilitate the invasion of human red blood cells and may explain, at least in part, the basis of the recent zoonotic infections.
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