Plasmodium cynomolgi genome sequences provide insight into Plasmodium vivax and the monkey malaria clade

Tachibana, Shin Ichiro; Sullivan, Steven A.; Kawai, Shinya; Nakamura, Shota; Kim, Hyunjae R.; Goto, Naohisa; Arisue, Nobuko; Palacpac, Nirianne; Honma, Hajime; Yagi, Mamiko; Tougan, Takahiro; Katakai, Yuko; Kaneko, O.; Mita, Toshihiro; Kita, Kiyoshi; Yasutomi, Yasuhiro; Sutton, Patrick L.; Shakhbatyan, Rimma; Horii, Toshihiro; Yasunaga, Teruo; Barnwell, John W.; Escalante, Ananías A.; Carlton, Jane M.; Tanabe, Kazuyuki

doi:10.1038/ng.2375

Cited by 176 publications

(210 citation statements)

References 36 publications

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“…Unlike P. vivax, most of the proposed P. cynomolgi gene models for msp7 include introns (Tachibana et al, 2012), for example, the paralogs PCYB_122740, PCYB_122750, PCYB_122770, PCYB_122780, and PCYB_122800. Yet, the sequences for those P. cynomolgi paralogs are in reading frame and can be aligned with their orthologs in P. vivax .…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies have shown that there is large variation in the number and composition of paralogs of the msp7 family among Plasmodium species (Garzón-Ospina et al, 2010; Kadekoppala and Holder, 2010). In particular, an expansion of the msp7 multigene family was suggested to have occurred in P. vivax and its closest related species found in Southeast Asian macaques, Plasmodium cynomolgi (Mongui et al, 2006; Tachibana et al, 2012). However, limited information on other species within that clade did not allow for further exploration of this pattern.…”

Section: Introductionmentioning

confidence: 99%

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Evolution of the merozoite surface protein 7 ( msp7 ) family in Plasmodium vivax and P . falciparum : A comparative approach

Castillo

Pacheco

Escalante

2017

Infection, Genetics and Evolution

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Malaria parasites (genus Plasmodium) are a diverse group found in many species of vertebrate hosts. These parasites invade red blood cells in a complex process comprising several proteins, many encoded by multigene families, one of which is merozoite surface protein-7 (msp7). In the case of Plasmodium vivax, the most geographically widespread human-infecting species, differences in the number of paralogs within multigene families have been previously explained, at least in part, as potential adaptations to the human host. To investigate this in msp7, we studied its orthologs in closely related nonhuman primate parasites; investigating both paralog evolutionary history and genetic polymorphism. The emerging patterns were then compared with the human parasite Plasmodium falciparum. We found that the evolution of the msp7 family is consistent with a birth-and-death model, where duplications, pseudogenizations, and gene loss events are common. However, all paralogs in P. vivax and P. falciparum had orthologs in their closely related species in non-human primates indicating that the ancestors of those paralogs precede the events leading to their origins as human parasites. Thus, the number of paralogs cannot be explained as an adaptation to human hosts. Although there is no functional information for msp7 in P. vivax, we found evidence for purifying selection in the genetic polymorphism of some of its paralogs as well as their orthologs in closely related non-human primate parasites. We also found evidence indicating that a few of P. vivax’s paralogs may have diverged from their orthologs in non-human primates by episodic positive selection. Hence, they may had been under selection when the lineage leading to P. vivax diverged from the Asian non-human primates and switched into Homininae. All these lines of evidence suggest that msp7 is functionally important in P. vivax.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Evolution of the merozoite surface protein 7 ( msp7 ) family in Plasmodium vivax and P . falciparum : A comparative approach

Castillo

Pacheco

Escalante

2017

Infection, Genetics and Evolution

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“…Orthologs of the P. knowlesi RBLs are present in P. vivax (35,36), but, given that our data indicate the P. knowlesi NBPXa protein is functional in invasion of both normocytes and reticulocytes, it is tempting to speculate that the absence of this protein in P. vivax could account for the parasite's restriction to reticulocytes. Intriguingly another closely related simian malaria parasite, P. cynomolgi, contains orthologs for RBL proteins specific for both P. vivax and P. knowlesi (11,37). Transferring orthologs from P. vivax or P. cynomolgi into P. knowlesi may offer opportunities to study both the requirements for and the evolution of P. vivax invasion.…”

Section: Discussionmentioning

confidence: 99%

Normocyte-binding protein required for human erythrocyte invasion by the zoonotic malaria parasite Plasmodium knowlesi

Moon

Sharaf

Hastings

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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The dominant cause of malaria in Malaysia is now Plasmodium knowlesi, a zoonotic parasite of cynomolgus macaque monkeys found throughout South East Asia. Comparative genomic analysis of parasites adapted to in vitro growth in either cynomolgus or human RBCs identified a genomic deletion that includes the gene encoding normocyte-binding protein Xa (NBPXa) in parasites growing in cynomolgus RBCs but not in human RBCs. Experimental deletion of the NBPXa gene in parasites adapted to growth in human RBCs (which retain the ability to grow in cynomolgus RBCs) restricted them to cynomolgus RBCs, demonstrating that this gene is selectively required for parasite multiplication and growth in human RBCs. NBPXa-null parasites could bind to human RBCs, but invasion of these cells was severely impaired. Therefore, NBPXa is identified as a key mediator of P. knowlesi human infection and may be a target for vaccine development against this emerging pathogen.

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“…Our data support the use of this parasite-host combination to study the molecular mechanisms involved in the pathogenesis of severe malaria. Finally, it is worth noting that other simian Plasmodium species such P. cynomolgi, a parasite biologically and phylogenetically closer to P. vivax (131), offers a unique opportunity for future comparative and coinfection studies to better understand the complex parasite-host pathophysiological interactions that operate in human and nonhuman primate malaria infections. We are grateful for the contributions of Eileen Breding, Stephanie Ehnert, Christopher Souder, and all the veterinary staff at the Yerkes National Primate Research Center.…”

Section: Fig 11mentioning

confidence: 99%

Plasmodium coatneyi in Rhesus Macaques Replicates the Multisystemic Dysfunction of Severe Malaria in Humans

et al. 2013

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f Severe malaria, a leading cause of mortality among children and nonimmune adults, is a multisystemic disorder characterized by complex clinical syndromes that are mechanistically poorly understood. The interplay of various parasite and host factors is critical in the pathophysiology of severe malaria. However, knowledge regarding the pathophysiological mechanisms and pathways leading to the multisystemic disorders of severe malaria in humans is limited. Here, we systematically investigate infections with Plasmodium coatneyi, a simian malaria parasite that closely mimics the biological characteristics of P. falciparum, and develop baseline data and protocols for studying erythrocyte turnover and severe malaria in greater depth. We show that rhesus macaques (Macaca mulatta) experimentally infected with P. coatneyi develop anemia, coagulopathy, and renal and metabolic dysfunction. The clinical course of acute infections required suppressive antimalaria chemotherapy, fluid support, and whole-blood transfusion, mimicking the standard of care for the management of severe malaria cases in humans. Subsequent infections in the same animals progressed with a mild illness in comparison, suggesting that immunity played a role in reducing the severity of the disease. Our results demonstrate that P. coatneyi infection in rhesus macaques can serve as a highly relevant model to investigate the physiological pathways and molecular mechanisms of malaria pathogenesis in naïve and immune individuals. Together with high-throughput postgenomic technologies, such investigations hold promise for the identification of new clinical interventions and adjunctive therapies.

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Plasmodium cynomolgi genome sequences provide insight into Plasmodium vivax and the monkey malaria clade

Cited by 176 publications

References 36 publications

Evolution of the merozoite surface protein 7 ( msp7 ) family in Plasmodium vivax and P . falciparum : A comparative approach

Evolution of the merozoite surface protein 7 ( msp7 ) family in Plasmodium vivax and P . falciparum : A comparative approach

Normocyte-binding protein required for human erythrocyte invasion by the zoonotic malaria parasite Plasmodium knowlesi

Plasmodium coatneyi in Rhesus Macaques Replicates the Multisystemic Dysfunction of Severe Malaria in Humans

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