The genome of the zoonotic malaria parasite Plasmodium simium reveals adaptations to host-switching
de Alvarenga, Denise Anete Madureira
de Pina-Costa, Anielle
Guzmán-Vega, Francisco J.
de Abreu, Filipe Vieira Santos
Júnior, Cesare Bianco
Junior, Julio Cesar de Souza
Moreira, Silvia Bahadian
Hirano, Zelinda Maria Braga
Ferreira-da-Cruz, Maria de Fátima
de Oliveira, Ricardo Lourenço
Arold, Stefan T.
Jeffares, Daniel C.
de Brito, Cristiana Ferreira Alves
Daniel-Ribeiro, Cláudio Tadeu
KAUST DepartmentBiological and Environmental Sciences and Engineering (BESE) Division
Computational Bioscience Research Center (CBRC)
Computer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
Pathogen Genomics Laboratory
Structural Biology and Engineering
KAUST Grant NumberURF/1/1976
Permanent link to this recordhttp://hdl.handle.net/10754/664279
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AbstractSummaryPlasmodium simium, a malaria parasite of non-human primates in the Atlantic forest region of Brazil was recently shown to cause zoonotic infections in humans. Phylogenetic analyses based on the whole genome sequences of six P. simium isolates from humans and two isolates from brown howler monkeys revealed that P. simium is monophyletic within the broader diversity of South American Plasmodium vivax, consistent with the hypothesis that P. simium first infected non-human primates as a result of a host-switch of P. vivax from humans. Very low levels of genetic diversity within P. simium and the absence of P. simium-P. vivax hybrids suggest that the P. simium population emerged recently with a subsequent period of independent evolution in Platyrrhini monkeys. We find that Plasmodium Interspersed Repeat (PIR) genes, Plasmodium Helical Interspersed Subtelomeric (PHIST) genes and Tryptophan-Rich Antigen (TRAg) genes in P. simium are divergent from P. vivax orthologues and are enriched for non-synonymous single nucleotide polymorphisms, consistent with the rapid evolution of these genes. Analysis of genes involved in erythrocyte invasion revealed several notable differences between P. vivax and P. simium, including large deletions within the coding region of the Duffy Binding Protein 1 (DBP1) and Reticulocyte Binding Protein 2a (RBP2a) genes of P. simium. Sequence analysis of P. simium isolates from non-human primates (NHPs) and zoonotic human infections revealed a deletion of 38 amino acids in DBP1 present in all human-derived isolates, whereas NHP isolates were multi-allelic at this locus. We speculate that these deletions in key erythrocyte invasion ligands along with other significant genetic changes may have facilitated zoonotic transfer to humans. NHPs are a reservoir of parasites potentially infectious to humans that must be considered in malaria eradication efforts. The P. simium genome is an important resource for understanding the mechanisms of malaria parasite zoonoses.
CitationMourier, T., de Alvarenga, D. A. M., Kaushik, A., de Pina-Costa, A., Douvropoulou, O., Guan, Q., … Pain, A. (2019). The genome of the zoonotic malaria parasite Plasmodium simium reveals adaptations to host-switching. doi:10.1101/841171
SponsorsThe work was supported financially by the King Abdullah University of Science and Technology (KAUST) through the baseline fund BRF1020/01/01 to AP and BAS/1/1056-01-01 to STA, and the Award No. URF/1/1976-25 from the Office of Sponsored Research (OSR). The field work in the Atlantic Forest and laboratory analysis in Brazil received financial support from the Secretary for Health Surveillance of the Ministry of Health through the Global Fund (agreement IOC-005-Fio-13), Programa Nacional de Excelência (PRONEX) and contract 407873/2018-0 of the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), the Fundação de Amparo à Pesquisa do Estado de Minas Gerais (Fapemig CBB-APQ-02620-15) and the Fundação Carlos Chagas Filho de Amparo Pesquisa do Estado do Rio de Janeiro (Faperj), Brazil. CNPq supports CFAB, CTDR,MFFC, PB and RLO, with a research productivity fellowship. CTDR (CNE: E-26/202.921/2018), MFFC, PB and RLO are also supported by Faperj as Cientistas do nosso estado. AdP-C was supported by a postdoctoral fellowship from the Faperj and DAMA by a fellowship from the CGZV-SVS (Brazilian Ministry of Health) TED 49/2018 grant. SF was supported by a Wellcome Seed Award in Science to DCJ (208965/Z/17/Z).
PublisherCold Spring Harbor Laboratory
Except where otherwise noted, this item's license is described as Archived with thanks to Cold Spring Harbor Laboratory