Agarwal A, Guindo A, Cissoko Y, Taylor JG, Coulibaly D, Kone A, Kayentao K, Djimde A, Plowe CV, Doumbo O, Wellems TE, Diallo D, 2000. Hemoglobin C associated with protection from severe malaria in the Dogon of Mali, a west African population with a low prevalence of hemoglobin S. Blood 96: 2358–2363.
Modiano D, Luoni G, Sirima BS, Simpore J, Verra F, Konate A, Rastrelli E, Olivieri A, Calissano C, Paganotti GM, D'Urbano L, Sanou I, Sawadogo A, Modiano G, Coluzzi M, 2001. Haemoglobin C protects against clinical Plasmodium falciparum malaria. Nature 414: 305–308.
Mockenhaupt FP, Ehrhardt S, Cramer JP, Otchwemah RN, Anemana SD, Goltz K, Mylius F, Dietz E, Eggelte TA, Bienzle U, 2004. Hemoglobin C and resistance to severe malaria in Ghanaian children. J Infect Dis 190: 1006–1009.
May J, Evans JA, Timmann C, Ehmen C, Busch W, Thye T, Agbenyega T, Horstmann RD, 2007. Hemoglobin variants and disease manifestations in severe falciparum malaria. JAMA 297: 2220–2226.
Williams TN, Mwangi TW, Wambua S, Alexander ND, Kortok M, Snow RW, Marsh K, 2005. Sickle cell trait and the risk of Plasmodium falciparum malaria and other childhood diseases. J Infect Dis 192: 178–186.
Fucharoen S, Winichagoon P, 1987. Hemoglobinopathies in southeast Asia. Hemoglobin 11: 65–88.
Naka I, Ohashi J, Nuchnoi P, Hananantachai H, Looareesuwan S, Tokunaga K, Patarapotikul J, 2008. Lack of association of the HbE variant with protection from cerebral malaria in Thailand. Biochem Genet 46: 708–711.
Williams TN, 2006. Human red blood cell polymorphisms and malaria. Curr Opin Microbiol 9: 388–394.
Ohashi J, Naka I, Patarapotikul J, Hananantachai H, Brittenham G, Looareesuwan S, Clark AG, Tokunaga K, 2004. Extended linkage disequilibrium surrounding the hemoglobin E variant due to malarial selection. Am J Hum Genet 74: 1198–1208.
Haldane J, 1949. The rate of mutation of human genes. Hereditas 35: 267–273.
Hutagalung R, Wilairatana P, Looareesuwan S, Brittenham GM, Aikawa M, Gordeuk VR, 1999. Influence of hemoglobin E trait on the severity of falciparum malaria. J Infect Dis 179: 283–286.
Oo M, Tin S, Marlar T, O'Sullivan WJ, 1995. Genetic red cell disorders and severity of falciparum malaria in Myanmar. Bull World Health Organ 73: 659–665.
Hutagalung R, Wilairatana P, Looareesuwan S, Brittenham GM, Gordeuk VR, 2000. Influence of hemoglobin E trait on the antimalarial effect of artemisinin derivatives. J Infect Dis 181: 1513–1516.
Ahmed S, Galagan S, Scobie H, Khyang J, Prue CS, Khan WA, Ram M, Alam MS, Haq MZ, Akter J, Glass G, Norris DE, Nyunt MM, Shields T, Sullivan DJ, Sack DA, 2013. Malaria hotspots drive hypoendemic transmission in the Chittagong Hill Districts of Bangladesh. PLoS One 8: e69713.
Khan WA, Sack DA, Ahmed S, Prue CS, Alam MS, Haque R, Khyang J, Ram M, Akter J, Nyunt MM, Norris D, Glass G, Shields T, Haq MZ, Cravioto A, Sullivan DJ Jr, 2011. Mapping hypoendemic, seasonal malaria in rural Bandarban, Bangladesh: a prospective surveillance. Malar J 10: 124.
Khim N, Benedet C, Kim S, Kheng S, Siv S, Leang R, Lek S, Muth S, Chea N, Chuor CM, Duong S, Kerleguer A, Tor P, Chim P, Canier L, Witkowski B, Taylor WR, Menard D, 2013. G6PD deficiency in Plasmodium falciparum and Plasmodium vivax malaria-infected Cambodian patients. Malar J 12: 171.
Team RR, 2008. A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing.
Alperin JB, Dow PA, Petteway MB, 1977. Hemoglobin-A2 levels in health and various hematologic disorders. Am J Clin Pathol 67: 219–226.
Billo MA, Johnson ES, Doumbia SO, Poudiougou B, Sagara I, Diawara SI, Diakite M, Diallo M, Doumbo OK, Tounkara A, Rice J, James MA, Krogstad DJ, 2012. Sickle cell trait protects against Plasmodium falciparum infection. Am J Epidemiol 176 (Suppl 7): S175–S185.
Ashley EA, Dhorda M, Fairhurst RM, Amaratunga C, Lim P, Suon S, Sreng S, Anderson JM, Mao S, Sam B, Sopha C, Chuor CM, Nguon C, Sovannaroth S, Pukrittayakamee S, Jittamala P, Chotivanich K, Chutasmit K, Suchatsoonthorn C, Runcharoen R, Hien TT, Thuy-Nhien NT, Thanh NV, Phu NH, Htut Y, Han KT, Aye KH, Mokuolu OA, Olaosebikan RR, Folaranmi OO, Mayxay M, Khanthavong M, Hongvanthong B, Newton PN, Onyamboko MA, Fanello CI, Tshefu AK, Mishra N, Valecha N, Phyo AP, Nosten F, Yi P, Tripura R, Borrmann S, Bashraheil M, Peshu J, Faiz MA, Ghose A, Hossain MA, Samad R, Rahman MR, Hasan MM, Islam A, Miotto O, Amato R, MacInnis B, Stalker J, Kwiatkowski DP, Bozdech Z, Jeeyapant A, Cheah PY, Sakulthaew T, Chalk J, Intharabut B, Silamut K, Lee SJ, Vihokhern B, Kunasol C, Imwong M, Tarning J, Taylor WJ, Yeung S, Woodrow CJ, Flegg JA, Das D, Smith J, Venkatesan M, Plowe CV, Stepniewska K, Guerin PJ, Dondorp AM, Day NP, White NJ, 2014. Spread of artemisinin resistance in Plasmodium falciparum malaria. N Engl J Med 371: 411–423.
Starzengruber P, Swoboda P, Fuehrer HP, Khan WA, Hofecker V, Siedl A, Fally M, Graf O, Teja-Isavadharm P, Haque R, Ringwald P, Noedl H, 2012. Current status of artemisinin-resistant falciparum malaria in south Asia: a randomized controlled artesunate monotherapy trial in Bangladesh. PLoS One 7: e52236.
Noedl H, Se Y, Schaecher K, Smith BL, Socheat D, Fukuda MM, Consortium AS, 2008. Evidence of artemisinin-resistant malaria in western Cambodia. N Engl J Med 359: 2619–2620.
Noedl H, Se Y, Sriwichai S, Schaecher K, Teja-Isavadharm P, Smith B, Rutvisuttinunt W, Bethell D, Surasri S, Fukuda MM, Socheat D, Thap LC, 2010. Artemisinin resistance in Cambodia: a clinical trial designed to address an emerging problem in southeast Asia. Clin Infect Dis 51: E82–E89.
Li QG, O'Neil M, Xie LS, Caridha D, Zeng Q, Zhang J, Pybus B, Hickman M, Melendez V, 2014. Assessment of the prophylactic activity and pharmacokinetic profile of oral tafenoquine compared to primaquine for inhibition of liver stage malaria infections. Malar J 13: 141.
Fernando D, Rodrigo C, Rajapakse S, 2011. Primaquine in vivax malaria: an update and review on management issues. Malar J 10: 351.
Global Malaria Programme, 2012. Single Dose Primaquine as a Gametocytocide in Plasmodium falciparum Malaria. Available at: http://www.who.int/malaria/mpac/sep2012/en/.
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Hemoglobin E is largely confined to south and southeast Asia. The association between hemoglobin E (HbE) and malaria is less clear than that of hemoglobin S and C. As part of a malaria study in the Chittagong Hill Districts of Bangladesh, an initial random sample of 202 individuals showed that 39% and 49% of Marma and Khyang ethnic groups, respectively, were positive for either heterozygous or homozygous hemoglobin E. In this group, 6.4% were also found to be severely deficient and 35% mildly deficient for glucose-6-phosphate dehydrogenase (G6PD). In a separate Plasmodium falciparum malaria case–uninfected control study, the odds of having homozygous hemoglobin E (HbEE) compared with normal hemoglobin (HbAA) were higher among malaria cases detected by passive surveillance than age and location matched uninfected controls (odds ratio [OR] = 5.0, 95% confidence interval [CI] = 1.07–46.93). The odds of heterozygous hemoglobin E (HbAE) compared with HbAA were similar between malaria cases and uninfected controls (OR = 0.71, 95% CI = 0.42–1.19). No association by hemoglobin type was found in the initial parasite density or the proportion parasite negative after 2 days of artemether/lumefantrine treatment. HbEE, but not HbAE status was associated with increased passive case detection of malaria.
Financial support: This study was funded by Johns Hopkins Malaria Research Institute at the Johns Hopkins Bloomberg School of Public Health (grant no. 00679) and the Johns Hopkins MSTP program and Johns Hopkins Department of International Health for providing funding to Kerry L. Shannon. The icddr,b also gratefully acknowledges the following donors, which provide unrestricted support to the Center's research efforts: the Australian Agency for International Development (AusAID), the Government of the People's Republic of Bangladesh, the Canadian International Development Agency (CIDA), the Swedish International Development Cooperation Agency (SIDA), and the Department for International Development, United Kingdom (DFID). We are also indebted to the Johns Hopkins Center for Global Health and John Snow, Inc., who provided travel funding for a student investigator.
Authors' addresses: Kerry L. Shannon, Malathi Ram, and David A. Sack, Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, E-mails: firstname.lastname@example.org, email@example.com, and firstname.lastname@example.org. Sabeena Ahmed, Hafizur Rahman, Ashish Chowdhury, Chai Shwai Prue, Jacob Khyang, M. Zahirul Haq, Jasmin Akter, and Wasif A. Khan, Centre for Population, Urbanization and Climate Change, icddr,b, Dhaka, Bangladesh, E-mails: email@example.com, firstname.lastname@example.org, email@example.com, firstname.lastname@example.org, email@example.com, firstname.lastname@example.org, and email@example.com. Gregory E. Glass, Department of Geography, Emerging Pathogens Institute, University of Florida, Gainesville, FL, E-mail: firstname.lastname@example.org. Timothy Shields and David J. Sullivan Jr., Department of Molecular Microbiology and Immunology, Johns Hopkins Malaria Research Institute, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, E-mails: email@example.com and firstname.lastname@example.org. Myaing M. Nyunt, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, E-mail: email@example.com.