Reduced Risk of Plasmodium vivax Malaria in Papua New Guinean Children with Southeast Asian Ovalocytosis in Two Cohorts and a Case-Control Study

Rosanas-Urgell, Anna; Lin, Enmoore; Manning, Laurens; Rarau, Patricia; Laman, Moses; Senn, Nicolas; Grimberg, Brian T.; Tavul, Livingstone; Stanisic, Danielle I.; Robinson, Leanne J.; Aponte, John J.; Dabod, Elijah; Reeder, John C.; Siba, Peter; Zimmerman, Peter A.; Davis, Timothy M. E.; King, Christopher L.; Michon, P; Müeller, Ivo

doi:10.1371/journal.pmed.1001305

Cited by 56 publications

(54 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…FY*B/FY*X and FY*A/FY*X genotypes are associated with low parasite density, which may favorably impact hemoglobin levels (69). Observational studies have shown protection against P. vivax infections conferred by a RBC enzyme (glucose-6-phosphate dehydrogenase) deficiency (70)(71)(72) and an erythrocyte membrane disorder (Southeast Asian ovalocytosis) by a mechanism that is independent of the Duffy antigen (73). On the other hand, thalassemias, which are disorders of globin synthesis, appear to increase the susceptibility to vivax malaria in carrier populations from different geographic regions (74)(75)(76)(77).…”

Section: Overview Of the Major Determinants Of Vivax Anemiamentioning

confidence: 99%

Potential Immune Mechanisms Associated with Anemia in Plasmodium vivax Malaria: a Puzzling Question

et al. 2014

View full text Add to dashboard Cite

The pathogenesis of malaria is complex, generating a broad spectrum of clinical manifestations. One of the major complications and concerns in malaria is anemia, which is responsible for considerable morbidity in the developing world, especially in children and pregnant women. Despite its enormous health importance, the immunological mechanisms involved in malaria-induced anemia remain incompletely understood. Plasmodium vivax, one of the causative agents of human malaria, is known to induce a strong inflammatory response with a robust production of immune effectors, including cytokines and antibodies. Therefore, it is possible that the extent of the immune response not only may facilitate the parasite killing but also may provoke severe illness, including anemia. In this review, we consider potential immune effectors and their possible involvement in generating this clinical outcome during P. vivax infections.

show abstract

Section: Overview Of the Major Determinants Of Vivax Anemiamentioning

confidence: 99%

Potential Immune Mechanisms Associated with Anemia in Plasmodium vivax Malaria: a Puzzling Question

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Although most research has focused on P. falciparum (especially with sickle-cell disease), some polymorphisms have been found to confer protection against P. vivax . For instance, southeast Asian ovalocytosis in Papua New Guinea may confer partial resistance to infection,104,105 as may certain variants of G6PD deficiency 70,106,107. In contrast, both alpha and beta thalassemia have been associated with increased risk of P. vivax parasitemia 108,109.…”

Section: High-risk Groupsmentioning

confidence: 99%

Global Epidemiology of Plasmodium vivax

Howes¹,

Battle²,

Mendis³

et al. 2016

Am J Trop Med Hyg

326

257

View full text Add to dashboard Cite

Plasmodium vivax is the most widespread human malaria, putting 2.5 billion people at risk of infection. Its unique biological and epidemiological characteristics pose challenges to control strategies that have been principally targeted against Plasmodium falciparum. Unlike P. falciparum, P. vivax infections have typically low blood-stage parasitemia with gametocytes emerging before illness manifests, and dormant liver stages causing relapses. These traits affect both its geographic distribution and transmission patterns. Asymptomatic infections, high-risk groups, and resulting case burdens are described in this review. Despite relatively low prevalence measurements and parasitemia levels, along with high proportions of asymptomatic cases, this parasite is not benign. Plasmodium vivax can be associated with severe and even fatal illness. Spreading resistance to chloroquine against the acute attack, and the operational inadequacy of primaquine against the multiple attacks of relapse, exacerbates the risk of poor outcomes among the tens of millions suffering from infection each year. Without strategies accounting for these P. vivax-specific characteristics, progress toward elimination of endemic malaria transmission will be substantially impeded.

show abstract

“…Results from this study showed that in a cohort of infants 3–21 months of age SAO was associated with a 55% reduction in the risk of clinical P. vivax episodes with parasitaemia greater than 500 infected cells/μl (adjusted IRR (incidence rate ratio) = 0.54; CI 95 (0.34, 0.59), P < 0.0001). Additionally, in a treatment-time to re-infection cohort of 5–14 year olds, SAO children experienced a 52% reduction in P. vivax re-infection diagnosed by light microscopy (CI 95 (23, 87), P = 0.014) (Rosanas-Urgell et al, 2012). Further studies showed that while Duffy antigen expression was not significantly different on SAO compared to normal erythrocytes, high-level PvDBP-specific binding inhibitory antibodies (>90% binding inhibition) were observed significantly more often in sera from SAO than non-SAO children (SAO, 22.2%; non-SAO, 6.7%; P = 0.008)(Rosanas-Urgell et al, 2012).…”

Section: Evolving Perspectives On Resistance To P Vivaxmentioning

confidence: 99%

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Zimmerman

Ferreira

Howes

et al. 2013

Advances in Parasitology

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Reduced Risk of Plasmodium vivax Malaria in Papua New Guinean Children with Southeast Asian Ovalocytosis in Two Cohorts and a Case-Control Study

Cited by 56 publications

References 51 publications

Potential Immune Mechanisms Associated with Anemia in Plasmodium vivax Malaria: a Puzzling Question

Potential Immune Mechanisms Associated with Anemia in Plasmodium vivax Malaria: a Puzzling Question

Global Epidemiology of Plasmodium vivax

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Contact Info

Product

Resources

About