A Parasite Resembling<i>Plasmodium Falciparum</i>in a Chimpanzee

Blacklock, B.; Adler, S.

doi:10.1080/00034983.1922.11684303

Cited by 45 publications

(33 citation statements)

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“…Our data show not only that PfEBA-175 prefers Neu5Ac but also that Neu5Gc interferes with this binding, likely explaining why P. falciparum is unable to successfully infect healthy chimpanzees. Conversely, PrEBA-175 strongly prefers Neu5Gc, perhaps explaining why P. reichenowi failed to infect human subjects in old studies (11,12). The impact of merozoite invasion ligands on host species specificity has been confirmed recently in the simian malaria, Plasmodium knowlesi, in which knockout of P. knowlesi DBP-␣, an invasion ligand related to EBA-175, renders that parasite unable to invade human erythrocytes (53).…”

Section: Discussionmentioning

confidence: 99%

“…falciparum and P. reichenowi are two morphologically indistinguishable Plasmodium species that nevertheless exhibit strong host preferences for humans and chimpanzees, respectively (11,12,15). Recent phylogenetic sequence studies have confirmed the genetic distinctness of these species.…”

Section: Discussionmentioning

confidence: 99%

“…showed that humans could not be infected with parasitized chimpanzee blood (11,12). Conversely, chimpanzees were not successfully infected with blood from humans suffering from P. falciparum parasitemia (12).…”

mentioning

confidence: 99%

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Evolution of human-chimpanzee differences in malaria susceptibility: Relationship to human genetic loss of N -glycolylneuraminic acid

Martı́n

Rayner

Gagneux

et al. 2005

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

187

178

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Chimpanzees are the closest evolutionary cousins of humans, sharing >99% identity in most protein sequences. Plasmodium falciparum is the major worldwide cause of malaria mortality. Plasmodium reichenowi, a morphologically identical and genetically very similar parasite, infects chimpanzees but not humans. Conversely, experimental P. falciparum infection causes brief moderate parasitization and no severe infection in chimpanzees. This surprising host specificity remains unexplained. We modified and enhanced traditional methods for measuring sialic acid (Sia)-dependent recognition of glycophorins by merozoite erythrocyte-binding proteins, eliminating interference caused by endogenous Sias on transfected cells, and by using erythroleukemia cells to allow experimental manipulation of Sia content. We present evidence that these remarkable differences among such closely related host-parasite pairs is caused by species-specific erythrocyte-recognition profiles, apparently related to the human-specific loss of the common primate Sia N-glycolylneuraminic acid. The major merozoite-binding protein erythrocyte-binding antigen-175 of P. falciparum apparently evolved to take selective advantage of the excess of the Sia N-acetylneuraminic acid (the precursor of N-glycolylneuraminic acid) on human erythrocytes. The contrasting preference of P. reichenowi erythrocyte-binding antigen-175 for N-glycolylneuraminic acid is likely the ancestral condition. The surprising ability of P. falciparum to cause disease in New World Aotus monkeys (geographically isolated from P. falciparum until arrival of peoples from the Old World) can be explained by parallel evolution of a human-like Sia expression pattern in these distantly related primates. These results also have implications for the prehistory of hominids and for the genetic origins and recent emergence of P. falciparum as a major human pathogen

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Evolution of human-chimpanzee differences in malaria susceptibility: Relationship to human genetic loss of N -glycolylneuraminic acid

Martı́n

Rayner

Gagneux

et al. 2005

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

187

178

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“…Despite the origin of P. falciparum as a zoonosis, and the continuing coexistence of humans and apes in West and Central Africa, extensive field studies have failed to detect P. falciparum in wild-living chimpanzees and gorillas (5). Although there are reports of P. falciparum infecting chimpanzees either in certain captive settings (2) or following splenectomy and deliberate transfer of P. falciparum-infected human blood (8)(9)(10), the resulting infections have low parasitemia and are not known to result in malignant tertian malaria, suggesting a host-specific barrier for replete infection. The existence of host-specific barriers within the Laverania subgenus is supported further by the strict host specificity exhibited by ape Laverania parasites in the wild: Plasmodium reichenowi, Plasmodium billcollinsi, and Plasmodium gaboni infect only chimpanzees, and Plasmodium praefalciparum, Plasmodium blacklocki, and Plasmodium adleri are restricted to gorillas (3)(4)(5)(6).…”

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confidence: 99%

RH5–Basigin interaction plays a major role in the host tropism of Plasmodium falciparum

Wanaguru¹,

Liu²,

Hahn

et al. 2013

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

137

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Plasmodium falciparum, the cause of almost all human malaria mortality, is a member of the Laverania subgenus which infects African great apes. Interestingly, Laverania parasites exhibit strict host specificity in their natural environment: P. reichenowi, P. billcollinsi, and P. gaboni infect only chimpanzees; P. praefalciparum, P. blacklocki, and P. adleri are restricted to gorillas, and P. falciparum is pandemic in humans. The molecular mechanism(s) responsible for these host restrictions are not understood, although the interaction between the parasite blood-stage invasion ligand EBA175 and the host erythrocyte receptor Glycophorin-A (GYPA) has been implicated previously. We reexamined the role of the EBA175-GYPA interaction in host tropism using recombinant proteins and biophysical assays and found that EBA175 orthologs from the chimpanzee-restricted parasites P. reichenowi and P. billcollinsi both bound to human GYPA with affinities similar to that of P. falciparum, suggesting that the EBA175-GYPA interaction is unlikely to be the sole determinant of Laverania host specificity. We next investigated the contribution of the recently discovered Reticulocyte-binding protein Homolog 5 (RH5)-Basigin (BSG) interaction in host-species selectivity and found that P. falciparum RH5 bound chimpanzee BSG with a significantly lower affinity than human BSG and did not bind gorilla BSG, mirroring the known host tropism of P. falciparum. Using site-directed mutagenesis, we identified residues in BSG that are responsible for the species specificity of PfRH5 binding. Consistent with the essential role of the PfRH5-BSG interaction in erythrocyte invasion, we conclude that species-specific differences in the BSG receptor provide a molecular explanation for the restriction of P. falciparum to its human host.surface plasmon resonance | protein interactions T he most deadly of the malaria parasites, Plasmodium falciparum, is highly divergent from the other species of Plasmodium known to infect humans (1-3), with its closest relatives comprising a group of chimpanzee and gorilla parasites from the subgenus Laverania (3-7). Despite the origin of P. falciparum as a zoonosis, and the continuing coexistence of humans and apes in West and Central Africa, extensive field studies have failed to detect P. falciparum in wild-living chimpanzees and gorillas (5). Although there are reports of P. falciparum infecting chimpanzees either in certain captive settings (2) or following splenectomy and deliberate transfer of P. falciparum-infected human blood (8-10), the resulting infections have low parasitemia and are not known to result in malignant tertian malaria, suggesting a host-specific barrier for replete infection. The existence of host-specific barriers within the Laverania subgenus is supported further by the strict host specificity exhibited by ape Laverania parasites in the wild: Plasmodium reichenowi, Plasmodium billcollinsi, and Plasmodium gaboni infect only chimpanzees, and Plasmodium praefalciparum, Plasmodium blacklocki, and Plasm...

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“…There is also evidence of intrauterine or transcolostral transmission [290,589,819]. Fatal cases of strongyloidiasis have been reported in the chimpanzee, gibbon, orangutan, patas monkey, and woolly monkey [50,51,171,176,228,360,422,504,526,571,636,650,677,857,861].…”

Section: Strongyloidiasismentioning

confidence: 99%

The Pathoparasitology of Nonhuman Primates: A Review

Toft¹

1986

Primates

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A Parasite ResemblingPlasmodium Falciparumin a Chimpanzee

Cited by 45 publications

References 0 publications

Evolution of human-chimpanzee differences in malaria susceptibility: Relationship to human genetic loss of N -glycolylneuraminic acid

Evolution of human-chimpanzee differences in malaria susceptibility: Relationship to human genetic loss of N -glycolylneuraminic acid

RH5–Basigin interaction plays a major role in the host tropism of Plasmodium falciparum

The Pathoparasitology of Nonhuman Primates: A Review

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