Plasmodium vivax and the Duffy antigen: A paradigm revisited

Mercereau‐Puijalon, Odile; Ménard, Didier

doi:10.1016/j.tracli.2010.06.005

Cited by 32 publications

(25 citation statements)

References 59 publications

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“…A body of empirical evidence is growing, however that P. vivax can infect and cause disease in Duffy negative individuals, as reported in Madagascar [76] and mainland sub-Saharan Africa [77]–[80] as well as outside Africa [81], [82]. Whether the invasion of erythrocytes via Duffy antigen-independent pathways is a newly evolved mechanism, or whether this capacity has been overlooked by the misdiagnosis of P. vivax in Africa as P. ovale remains unresolved [9], [42], [59]. Whilst this accumulated evidence stands contrary to our simplifying assumption of complete protection in Duffy negative individuals, there is currently no evidence to suggest that such infections are anything but rare and thus are unlikely to have any substantive influence on the epidemiology or infection prevalence of P. vivax at the population scale throughout most of Africa.…”

Section: Discussionmentioning

confidence: 99%

“…The parasitemia of P. vivax typically occurs at much lower densities compared to those of falciparum malaria, and successful detection by any given means of survey is much less likely. Another major driver of the global P. vivax landscape is the influence of the Duffy negativity phenotype [42]. This inherited blood condition confers a high degree of protection against P. vivax infection and is present at very high frequencies in the majority of African populations, although is rare elsewhere [43].…”

Section: Introductionmentioning

confidence: 99%

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A Long Neglected World Malaria Map: Plasmodium vivax Endemicity in 2010

et al. 2012

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BackgroundCurrent understanding of the spatial epidemiology and geographical distribution of Plasmodium vivax is far less developed than that for P. falciparum, representing a barrier to rational strategies for control and elimination. Here we present the first systematic effort to map the global endemicity of this hitherto neglected parasite.Methodology and FindingsWe first updated to the year 2010 our earlier estimate of the geographical limits of P. vivax transmission. Within areas of stable transmission, an assembly of 9,970 geopositioned P. vivax parasite rate (PvPR) surveys collected from 1985 to 2010 were used with a spatiotemporal Bayesian model-based geostatistical approach to estimate endemicity age-standardised to the 1–99 year age range (PvPR1–99) within every 5×5 km resolution grid square. The model incorporated data on Duffy negative phenotype frequency to suppress endemicity predictions, particularly in Africa. Endemicity was predicted within a relatively narrow range throughout the endemic world, with the point estimate rarely exceeding 7% PvPR1–99. The Americas contributed 22% of the global area at risk of P. vivax transmission, but high endemic areas were generally sparsely populated and the region contributed only 6% of the 2.5 billion people at risk (PAR) globally. In Africa, Duffy negativity meant stable transmission was constrained to Madagascar and parts of the Horn, contributing 3.5% of global PAR. Central Asia was home to 82% of global PAR with important high endemic areas coinciding with dense populations particularly in India and Myanmar. South East Asia contained areas of the highest endemicity in Indonesia and Papua New Guinea and contributed 9% of global PAR.Conclusions and SignificanceThis detailed depiction of spatially varying endemicity is intended to contribute to a much-needed paradigm shift towards geographically stratified and evidence-based planning for P. vivax control and elimination.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Long Neglected World Malaria Map: Plasmodium vivax Endemicity in 2010

et al. 2012

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“…For example, there are two antigens A and B produced by alleles FY*A and FY*B at the Duffy blood group locus [46,47]. Many African-Americans and Africans do not have either allele and have another allele, known generally as a Duffy null allele.…”

Section: Strength Of Selectionmentioning

confidence: 99%

Resistance to malaria in humans: the impact of strong, recent selection

Hedrick

2012

Malar J

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Malaria is one of the leading causes of death worldwide and has been suggested as the most potent type of selection in humans in recent millennia. As a result, genes involved in malaria resistance are excellent examples of recent, strong selection. In 1949, Haldane initially suggested that infectious disease could be a strong selective force in human populations. Evidence for the strong selective effect of malaria resistance includes the high frequency of a number of detrimental genetic diseases caused by the pleiotropic effects of these malaria resistance variants, many of which are “loss of function” mutants. Evidence that this selection is recent comes from the genetic dating of the age of a number of these malaria resistant alleles to less than 5,000 years before the present, generally much more recent than other human genetic variants. An approach to estimate selection coefficients from contemporary case–control data is presented. In the situations described here, selection is much greater than 1%, significantly higher than generally observed for other human genetic variation. With these selection coefficients, predictions are generated about the joint change of alleles S and C at the β-globin locus, and for α-thalassaemia haplotypes and S, variants that are unlinked but exhibit epistasis. Population genetics can be used to determine the amount and pattern of selection in the past and predict selection in the future for other malaria resistance variants as they are discovered.

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“…Some authors suggested that despite high frequencies of Duffy negativity, the frequency of Duffy positive blood groups (∼1%-5%) may be high enough to maintain a certain level of transmission of P. vivax in these areas (13,14). Alternatively, it has been proposed that P. vivax could use other pathways to enter human red blood cells and that Duffy negativity might no longer be a barrier to infection and transmission (12,15,16). Furthermore, Plasmodium ovale may have been misdiagnosed as P. vivax, given that the microscopic distinction of these two species is difficult (17).…”

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confidence: 99%

Diversity, host switching and evolution of Plasmodium vivax infecting African great apes

Prugnolle

Rougeron

Becquart

et al. 2013

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

119

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Plasmodium vivax is considered to be absent from Central and West Africa because of the protective effect of Duffy negativity. However, there are reports of persons returning from these areas infected with this parasite and observations suggesting the existence of transmission. Among the possible explanations for this apparent paradox, the existence of a zoonotic reservoir has been proposed. May great apes be this reservoir? We analyze the mitochondrial and nuclear genetic diversity of P. vivax parasites isolated from great apes in Africa and compare it to parasites isolated from travelers returning from these regions of Africa, as well as to human isolates distributed all over the world. We show that the P. vivax sequences from parasites of great apes form a clade genetically distinct from the parasites circulating in humans. We show that this clade's parasites can be infectious to humans by describing the case of a traveler returning from the Central African Republic infected with one of them. The relationship between this P. vivax clade in great apes and the human isolates is discussed.emergence | transfer | malaria | sylvatic | origin

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Plasmodium vivax and the Duffy antigen: A paradigm revisited

Cited by 32 publications

References 59 publications

A Long Neglected World Malaria Map: Plasmodium vivax Endemicity in 2010

A Long Neglected World Malaria Map: Plasmodium vivax Endemicity in 2010

Resistance to malaria in humans: the impact of strong, recent selection

Diversity, host switching and evolution of Plasmodium vivax infecting African great apes

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