The Impact of Phenotypic and Genotypic G6PD Deficiency on Risk of Plasmodium vivax Infection: A Case-Control Study amongst Afghan Refugees in Pakistan

Leslie, Toby; Briceño, Marnie; Mayan, Ismail; Mohammed, Nasir; Klinkenberg, Eveline; Sibley, Carol Hopkins; Whitty, Christopher J M; Rowland, Mark

doi:10.1371/journal.pmed.1000283

Cited by 83 publications

(99 citation statements)

References 30 publications

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“…Recently, evidence has suggested that G6PD deficiency caused by the Mahidol mutation in Southeast Asians provides parasite resistance to infection by P. vivax, but not to that by P. falciparum. Further, G6PD deficiency Med in Pakistan has been shown to provide protection from P. vivax malaria (Leslie et al, 2010).…”

Section: G6pd Deficiencymentioning

confidence: 99%

Population genetics of malaria resistance in humans

2011

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Section: G6pd Deficiencymentioning

confidence: 99%

Population genetics of malaria resistance in humans

2011

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“…G6PD is an important issue related to P. vivax malaria. A Mediterranean type of G6PD deficiency significantly protects against P. vivax infection among Afghan refugees in Pakistan (32). A similar report is also available for the G6PD Mahidol variant from Southeast Asia (33).…”

Section: Discussionmentioning

confidence: 75%

In Vivo Therapeutic Efficacy of Chloroquine Alone or in Combination with Primaquine against Vivax Malaria in Kolkata, West Bengal, India, and Polymorphism in pvmdr1 and pvcrt-o Genes

Ganguly¹,

Saha²,

Guha³

et al. 2013

Antimicrob Agents Chemother

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bPlasmodium vivax malaria, though benign, has now become a matter of concern due to recent reports of life-threatening severity and development of parasite resistance to different antimalarial drugs. The magnitude of the problem is still undetermined. The present study was undertaken to determine the in vivo efficacy of chloroquine (CQ) and chloroquine plus primaquine in P. vivax malaria in Kolkata and polymorphisms in the pvmdr1 and pvcrt-o genes. A total of 250 patients with P. vivax monoinfection were recruited and randomized into two groups, A and B; treated with chloroquine and chloroquine plus primaquine, respectively; and followed up for 42 days according to the WHO protocol of 2009. Data were analyzed using per-protocol analyses. T he burden of malaria caused by Plasmodium vivax has been greatly underappreciated in terms of both its clinical spectrum and incidence of disease (1, 2). P. vivax is the most widely distributed cause of malaria in the world; approximately 2.6 billion people are at risk, and 10 countries, including India, are at the highest risk of infection (3,4,5,6).P. vivax infections have been associated with mild symptoms, such as fever, headache, fatigue, chills, and musculoskeletal pain, and, in particular, paroxysms. Recently, however, severe complications, including renal failure, jaundice, acute respiratory distress syndrome, cerebral malaria, seizures, anemia, hyperparasitemia, thrombocytopenia, pulmonary edema, splenic rupture, and death, have been reported in exclusive association with P. vivax (7,8). The situation is further complicated by the emergence of resistance of the parasite to chloroquine (CQ).In most of the world, CQ remains the first-line treatment for patients with vivax malaria. In India, CQ was replaced by artemisinin combination therapy (ACT), a combination of artesunate and sulfadoxine-pyrimethamine, in 2010 for Plasmodium falciparum malaria, but for P. vivax malaria, CQ remains the first-line agent, along with primaquine (PQ) (0.25-mg/kg base) for 14 days under supervision or by detecting the glucose-6-phosphate dehydrogenase (G6PD) level. The first case of P. vivax resistance to CQ was reported in 1989 from Papua New Guinea (9). A higher rate of CQ-resistant P. vivax malaria, which exceeded 50%, was reported from different regions of Indonesia (10,11,12,13,14). Further sporadic cases were subsequently observed in the Philippines, Myanmar, Vietnam, Colombia, Guyana, and Turkey (15). Similar reports are also available from Madagascar (16) and Ethiopia (17). Despite these reports, it remains difficult to estimate the worldwide prevalence of P. vivax resistance to CQ. In India, the first case of CQ-resistant P. vivax malaria was reported from Assam in 1995 (18) and then in Mumbai (19) and Gujarat (20).The molecular mechanisms underlying CQ resistance in P. vivax malaria remain unknown and may involve multigenic loci, but two genes orthologous to the pfmdr1 and pfcrt genes that encode putative transporters, pvmdr1 (21) and pvcrt-o (22), have been suspected as possi...

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“…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

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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.

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The Impact of Phenotypic and Genotypic G6PD Deficiency on Risk of Plasmodium vivax Infection: A Case-Control Study amongst Afghan Refugees in Pakistan

Abstract: Analyses of a case-control study among Afghan refugees in Pakistan find that a G6PD (glucose-6-phosphate dehydrogenase) “Mediterranean” type deficiency confers substantial protection against Plasmodium vivax malaria.

Cited by 83 publications

References 30 publications

Population genetics of malaria resistance in humans

Population genetics of malaria resistance in humans

In Vivo Therapeutic Efficacy of Chloroquine Alone or in Combination with Primaquine against Vivax Malaria in Kolkata, West Bengal, India, and Polymorphism in pvmdr1 and pvcrt-o Genes

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

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