The Susceptibility of Liberians to the Madagascar Strain of Plasmodium vivax

Rs, Bray

doi:10.2307/3274317

Cited by 34 publications

(20 citation statements)

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“…When carefully controlled studies were performed in the context of malariotherapy, details showed that African-Americans and Africans consistently displayed significantly higher levels of resistance to P. vivax strains from numerous geographic origins and inoculation doses compared to Caucasians (Young et al, 1955). Additionally, because African-Americans from nonmalarious regions of the United States were as refractory to P. vivax infection as those from malarious regions, this resistance was suggested to be natural rather than acquired (Boyd and Stratman-Thomas, 1933; Becker et al, 1946; Young et al, 1946; Young et al, 1955; Bray, 1958). Of further interest, to determine if a P. vivax infection once established in an African-American patient would acquire characteristics enabling more successful infection of resistant individuals, Young et al used blood from a P. vivax -infected African-American to inoculate two resistant individuals of the same race (Young et al, 1955).…”

Section: The Era Of Great Biological Discoverymentioning

confidence: 99%

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Zimmerman

Ferreira

Howes

et al. 2013

Advances in Parasitology

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Resistance to Plasmodium vivax blood-stage infection has been widely recognised to result from absence of the Duffy (Fy) blood group from the surface of red blood cells (RBCs) in individuals of African descent. Interestingly, recent studies from different malaria-endemic regions have begun to reveal new perspectives on the association between Duffy gene polymorphism and P. vivax malaria. In Papua New Guinea and the Americas, heterozygous carriers of a Duffy-negative allele are less susceptible to P. vivax infection than Duffy-positive homozygotes. In Brazil, studies show that the Fya antigen, compared to Fyb, is associated with lower binding to the P. vivax Duffy-binding protein and reduced susceptibility to vivax malaria. Additionally, it is interesting that numerous studies have now shown that P. vivax can infect RBCs and cause clinical disease in Duffy-negative people. This suggests that the relationship between P. vivax and the Duffy antigen is more complex than customarily described. Evidence of P. vivax Duffy-independent red cell invasion indicates that the parasite must be evolving alternative red cell invasion pathways. In this chapter, we review the evidence for P. vivax Duffy-dependent and Duffy-independent red cell invasion. We also consider the influence of further host gene polymorphism associated with malaria endemicity on susceptibility to vivax malaria. The interaction between the parasite and the RBC has significant potential to influence the effectiveness of P. vivax-specific vaccines and drug treatments. Ultimately, the relationships between red cell polymorphisms and P. vivax blood-stage infection will influence our estimates on the population at risk and efforts to eliminate vivax malaria.

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Section: The Era Of Great Biological Discoverymentioning

confidence: 99%

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Zimmerman

Ferreira

Howes

et al. 2013

Advances in Parasitology

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“…Genetic diversity was assessed by Nei's unbiased expected heterozygosity (H e ) from haploid data and calculated as H e = [n/(n − 1)] [1 − ∑p 2 i ] (n is the number of isolates sampled; p i 2 is the frequency of the ith allele) (46). Population genetic differentiation between symptomatic Duffy negatives and positives was measured using Wright's F statistics (47); population genetic parameters were computed with FSTAT software, v2.9.4 (48).…”

Section: Methodsmentioning

confidence: 99%

“…erythrocyte | evolution | DARC | Madagascar D uring malaria fever therapy trials, performed to treat neurosyphilis (1920s to 1960s) and in experimental field trials, it was consistently demonstrated that Africans and African-Americans were highly resistant to Plasmodium vivax blood-stage malaria when challenged with human blood or mosquitoes infected with limited numbers of P. vivax strains (1)(2)(3). Following identification of the Duffy blood group (Fy; reviewed in Zimmerman, 2004) (4), population studies showed that individuals of African ancestry expressed neither Fy a nor Fy b antigens and were classified as Duffy negative, Fy(a−b−) (5).…”

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confidence: 99%

Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people

Ménard

Barnadas

Bouchier

et al. 2010

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

352

354

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Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*B ES /*B ES ) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffyindependent P. vivax invasion of human erythrocytes.erythrocyte | evolution | DARC | Madagascar

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“…It is well-known that Duffy-antigen expression on red blood cells is implicated in P. vivax susceptibility (Boyd and Stratman-Thomas, 1933;Bray, 1958;Miller et al, 1976). Recent studies indicate that Duffy-antigen expression is higher on reticulocytes (Woolley et al, 2000), that gametocyte production and infectivity in P. falciparum are higher in reticulocytotic blood, e.g., from sickle-cell anemics (Trager and Gill, 1992;Drakeley et al, 1999;Trager et al, 1999), that P. falciparum infectivity increases with the proportion of male gametocytes (Robert, Read et al, 1996), and that stimulation of erythropoesis, but not reticulocytosis per se, shifts gametocyte sex ratios in P. gallinaceum and P. vinckei toward males (Paul et al, 2000).…”

Section: Refers Explicitly Tomentioning

confidence: 99%

“…Earlier work reported that the mean oocyst density per mosquito increased with the density of microgametocytes (males) but not macrogametocytes (Boyd and Stratman-Thomas, 1932) and that the mean oocyst density and the proportion of mosquitoes infected tended to vary together (Boyd, 1942a). Boyd and Kitchen (1937) found microgametocyte density critical in the infectivity of P. vivax, but not of P. falciparum, and attributed the difference primarily to a higher overall gametocytemia required for successful P. falciparum transmission.It is well-known that Duffy-antigen expression on red blood cells is implicated in P. vivax susceptibility (Boyd and Stratman-Thomas, 1933;Bray, 1958;Miller et al, 1976). Recent studies indicate that Duffy-antigen expression is higher on reticulocytes (Woolley et al, 2000), that gametocyte production and infectivity in P. falciparum are higher in reticulocytotic blood, e.g., from sickle-cell anemics (Trager and Gill, 1992;Drakeley et al, 1999;Trager et al, 1999), that P. falciparum infectivity increases with the proportion of male gametocytes (Robert, Read et al, 1996), and that stimulation of erythropoesis, but not reticulocytosis per se, shifts gametocyte sex ratios in P. gallinaceum and P. vinckei toward males (Paul et al, 2000).…”

mentioning

confidence: 99%

Plasmodium vivax Blood-Stage Dynamics

McKenzie¹,

Jeffery²,

Collins³

2002

The Journal of Parasitology

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We examine the dynamics of parasitemia and gametocytemia reflected in the preintervention charts of 221 malaria-naive U.S. neurosyphilis patients infected with the St. Elizabeth strain of Plasmodium vivax, for malariatherapy, focusing on the 109 charts for which 15 or more days of patency preceded intervention and daily records encompassed an average 98% of the duration of each infection. Our approximations of merogony cycles (via "local peaks" in parasitemia) seldom fit patterns that correspond to "textbook" tertian brood structures. Peak parasitemia was higher in trophozoiteinduced infections than in sporozoite-induced ones. Relative densities of male and female gametocytes appeared to alternate, though without a discernably regular period. Successful transmission to mosquitoes did not depend on detectable gametocytemia or on absence of fever. When gametocytes were detected, transmission success depended on densities of only male gametocytes. Successful feeds occurred on average 4.7 days later in an infection than did failures. Parasitemia was lower in homologous reinfection, gametocytemia lower or absent.Plasmodium vivax asexual blood-stage cycles are authoritatively cited as displaying a period of 48 hr (Cox, 1993;Reisberg, 1997). Hence, a single-brood P. vivax infection would be expected to produce peaks of asexual parasitemia (in the form of merozoites) and corresponding fevers on alternate days and a 2-brood infection to produce daily (quotidian) peaks of parasitemia and fever. Whorton et al. (1947) attributed their observations of irregular or steady fevers to irregular parasite segmentation. Kitchen (1949) agreed, noting that the earliest phases of patent P. vivax infections might be marked by "continuous fever caused by more or less constant sporulation," but argued that "the great majority of the vivax plasmodia are segregated into two pyrogenic broods … whose corresponding developmental stages are separated by approximately twenty-four hours." Coatney et al. (1971) found P. vivax as often tertian as quotidian and remarked that "if the infection is allowed to run, it is not unusual for multiple broods to get-in-step resulting in a tertian fever pattern; likewise, tertian patterns, sometimes, become quotidian for a time, only to revert to tertian again." Garnham (1966) reported that "the process of schizogony in P. vivax is never of clockwork regularity." According to Shute (1958), "the true explanation is that the cycle depends on the patient and not on the parasite," meaning, in particular, that quotidian behavior marks the initial infection in a malaria-naive patient, whereas tertian behavior typifies relapses and subsequent infections.A companion paper on trophozoite-induced P. malariae infections addressed some of these phenomena (McKenzie et al., 2001). With the P. vivax charts, they can be addressed in the context of sporozoite-as well as trophozoite-induced infections. Inoculation modes may influence subsequent events: sporozoite-induced infections will show longer prepatency and incuba...

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The Susceptibility of Liberians to the Madagascar Strain of Plasmodium vivax

Cited by 34 publications

References 6 publications

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people

Plasmodium vivax Blood-Stage Dynamics

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