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5. SAA Isotypes in Patients with Secondary Amyloidosis

Author

Raynes, J. G., Hultquist, R., Molyneux, M., Griffin, G., McAdam, K. P. W. J., Natvig, Jacob B., editor, Førre, Øystein, editor, Husby, Gunnar, editor, Husebekk, Anne, editor, Skogen, Bjørn, editor, Sletten, Knut, editor, and Westermark, Per, editor

Published
1991
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18. HIV infection compounds the lymphopenia associated with cerebral malaria in Malawian children

Author

Mandala, W, Gondwe, E, Nyirenda, T, Drayson, M, Molyneux, M, and Maclennan, C

Subjects
wh_200, wc_503_5, HIV, virus diseases, wc_503, wa_320, wc_750, Journal of Blood Medicine, parasitic diseases, Malawian children, cerebral malaria, severe malarial anemia, Original Research, ws_100
Abstract

Wilson L Mandala,1–3 Esther N Gondwe,1,† Tonney S Nyirenda,1,4 Mark Drayson,5 Malcolm E Molyneux,1,6 Calman A MacLennan1,7 1Malawi Liverpool Wellcome Trust Clinical Research Programme, College of Medicine, Blantyre, Malawi; 2Biomedical Sciences Department, College of Medicine, Blantyre, Malawi; 3Academy of Medical Sciences, Malawi University of Science and Technology, Thyolo, Malawi; 4Pathology Department, College of Medicine, Blantyre, Malawi; 5Institute of Immunology and Immunotherapy, College of Medicine and Dental Sciences, University of Birmingham, Birmingham, UK; 6Liverpool School of Tropical Medicine, Liverpool, UK; 7Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK †Esther N Gondwe passed away on April 5, 2018 Aim: Cerebral malaria (CM), unlike severe malarial anemia (SMA), has previously been characterized by pan-lymphopenia that normalizes in convalescence, while HIV infection is associated with depletion of CD4+ T cells. In this study, we investigate whether HIV infection in Malawian children exacerbates the pan-lymphopenia associated with CM. Methods: We investigated the absolute and percentage lymphocyte-subset counts and their activation and memory status in Malawian children presenting with either CM who were HIV-uninfected (n=29), HIV-infected (n=9), or SMA who were HIV-uninfected (n=30) and HIV-infected (n=5) in comparison with HIV-uninfected children without malaria (n=42) and HIV-infected children without malaria (n=4). Results: HIV-infected CM cases had significantly lower absolute counts of T cells (P=0.006), CD4+ T cells (P=0.0008), and B cells (P=0.0014) than HIV-uninfected CM cases, and significantly lower percentages of CD4+ T cells than HIV-uninfected CM cases (P=0.005). HIV-infected SMA cases had significantly lower percentages of CD4+ T cells (P=0.001) and higher CD8+ T cells (P=0.003) in comparison with HIV-uninfected SMA cases. HIV-infected SMA cases had higher proportions of activated T cells (P=0.003) expressing CD69 than HIV-uninfected SMA cases. Conclusion: HIV infection compounds the perturbation of acute CM and SMA on lymphocytes, exacerbating subset-specific lymphopenia in CM and increasing activation status in SMA, potentially exacerbating host immunocompromise. Keywords: HIV, cerebral malaria, severe malarial anemia, Malawian children

Published
2019

22. Insights into malaria susceptibility using genome-wide data on 17,000 individuals from Africa, Asia and Oceania

Author

Band, G, Le, QS, Clarke, GM, Kivinen, K, Hubbart, C, Jeffreys, AE, Rowlands, K, Leffler, EM, Jallow, M, Conway, DJ, Sisay-Joof, F, Sirugo, G, d'Alessandro, U, Toure, OB, Thera, MA, Konate, S, Sissoko, S, Mangano, VD, Bougouma, EC, Sirima, SB, Amenga-Etego, LN, Ghansah, AK, Hodgson, AVO, Wilson, MD, Enimil, A, Ansong, D, Evans, J, Ademola, SA, Apinjoh, TO, Ndila, CM, Manjurano, A, Drakeley, C, Reyburn, H, Nguyen, HP, Nguyen, TNQ, Cao, QT, Tran, TH, Teo, YY, Manning, L, Laman, M, Michon, P, Karunajeewa, H, Siba, P, Allen, S, Allen, A, Bahlo, M, Davis, TME, Simpson, V, Shelton, J, Spencer, CCA, Busby, GBJ, Kerasidou, A, Drury, E, Stalker, J, Dilthey, A, Mentzer, AJ, McVean, G, Bojang, KA, Doumbo, O, Modiano, D, Koram, KA, Agbenyega, T, Amodu, OK, Achidi, E, Williams, TN, Marsh, K, Riley, EM, Molyneux, M, Taylor, T, Dunstan, SJ, Farrar, J, Mueller, I, Rockett, KA, Kwiatkowski, DP, Band, G, Le, QS, Clarke, GM, Kivinen, K, Hubbart, C, Jeffreys, AE, Rowlands, K, Leffler, EM, Jallow, M, Conway, DJ, Sisay-Joof, F, Sirugo, G, d'Alessandro, U, Toure, OB, Thera, MA, Konate, S, Sissoko, S, Mangano, VD, Bougouma, EC, Sirima, SB, Amenga-Etego, LN, Ghansah, AK, Hodgson, AVO, Wilson, MD, Enimil, A, Ansong, D, Evans, J, Ademola, SA, Apinjoh, TO, Ndila, CM, Manjurano, A, Drakeley, C, Reyburn, H, Nguyen, HP, Nguyen, TNQ, Cao, QT, Tran, TH, Teo, YY, Manning, L, Laman, M, Michon, P, Karunajeewa, H, Siba, P, Allen, S, Allen, A, Bahlo, M, Davis, TME, Simpson, V, Shelton, J, Spencer, CCA, Busby, GBJ, Kerasidou, A, Drury, E, Stalker, J, Dilthey, A, Mentzer, AJ, McVean, G, Bojang, KA, Doumbo, O, Modiano, D, Koram, KA, Agbenyega, T, Amodu, OK, Achidi, E, Williams, TN, Marsh, K, Riley, EM, Molyneux, M, Taylor, T, Dunstan, SJ, Farrar, J, Mueller, I, Rockett, KA, and Kwiatkowski, DP

Abstract

The human genetic factors that affect resistance to infectious disease are poorly understood. Here we report a genome-wide association study in 17,000 severe malaria cases and population controls from 11 countries, informed by sequencing of family trios and by direct typing of candidate loci in an additional 15,000 samples. We identify five replicable associations with genome-wide levels of evidence including a newly implicated variant on chromosome 6. Jointly, these variants account for around one-tenth of the heritability of severe malaria, which we estimate as ~23% using genome-wide genotypes. We interrogate available functional data and discover an erythroid-specific transcription start site underlying the known association in ATP2B4, but are unable to identify a likely causal mechanism at the chromosome 6 locus. Previously reported HLA associations do not replicate in these samples. This large dataset will provide a foundation for further research on thegenetic determinants of malaria resistance in diverse populations.

Published
2019

26. Averting a malaria disaster

Author

White, N J, Nosten, F, Looareesuwan, S, Watkins, W M, Marsh, K, Snow, R W, Kokwaro, G, Ouma, J, Hien, T T, Molyneux, M E, Taylor, T E, Newbold, C I, Ruebush, T K, Danis, M, Greenwood, B M, Anderson, R M, and Olliaro, P

Published
1999

35. Characterisation of the opposing effects of G6PD deficiency on cerebral malaria and severe malarial anaemia

Author

Clarke, GM, Rockett, K, Kivinen, K, Hubbart, C, Jeffreys, AE, Rowlands, K, Jallow, M, Conway, DJ, Bojang, KA, Pinder, M, Usen, S, Sisay-Joof, F, Sirugo, G, Toure, O, Thera, MA, Konate, S, Sissoko, S, Niangaly, A, Poudiougou, B, Mangano, VD, Bougouma, EC, Sirima, SB, Modioano, D, Amenga-Etego, LN, Ghansah, A, Koram, KA, Wilson, MD, Enimil, A, Evans, J, Amodu, OK, Olaniyan, S, Apinjoh, T, Mugri, R, Ndi, A, Ndila, CM, Uyoga, S, Macharia, A, Peshu, N, Williams, TN, Manjurano, A, Sepulveda, N, Clark, TG, Riley, E, Drakeley, C, Reyburn, H, Nyirongo, V, Kachala, D, Molyneux, M, Dunstan, SJ, Nguyen, HP, Nguyen, NQ, Cao, QT, Tran, TH, Manning, L, Laman, M, Siba, P, Karunajeewa, H, Allen, S, Allen, A, Davis, TME, Michon, P, Mueller, I, Molloy, SF, Campino, S, Kerasidou, A, Cornelius, VJ, Hart, L, Shah, SS, Band, G, Spencer, CCA, Agbenyega, T, Achidi, E, Doumbo, OK, Farrar, J, Marsh, K, Taylor, T, Kwaitkowski, DP, Clarke, GM, Rockett, K, Kivinen, K, Hubbart, C, Jeffreys, AE, Rowlands, K, Jallow, M, Conway, DJ, Bojang, KA, Pinder, M, Usen, S, Sisay-Joof, F, Sirugo, G, Toure, O, Thera, MA, Konate, S, Sissoko, S, Niangaly, A, Poudiougou, B, Mangano, VD, Bougouma, EC, Sirima, SB, Modioano, D, Amenga-Etego, LN, Ghansah, A, Koram, KA, Wilson, MD, Enimil, A, Evans, J, Amodu, OK, Olaniyan, S, Apinjoh, T, Mugri, R, Ndi, A, Ndila, CM, Uyoga, S, Macharia, A, Peshu, N, Williams, TN, Manjurano, A, Sepulveda, N, Clark, TG, Riley, E, Drakeley, C, Reyburn, H, Nyirongo, V, Kachala, D, Molyneux, M, Dunstan, SJ, Nguyen, HP, Nguyen, NQ, Cao, QT, Tran, TH, Manning, L, Laman, M, Siba, P, Karunajeewa, H, Allen, S, Allen, A, Davis, TME, Michon, P, Mueller, I, Molloy, SF, Campino, S, Kerasidou, A, Cornelius, VJ, Hart, L, Shah, SS, Band, G, Spencer, CCA, Agbenyega, T, Achidi, E, Doumbo, OK, Farrar, J, Marsh, K, Taylor, T, and Kwaitkowski, DP

Abstract

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is believed to confer protection against Plasmodium falciparum malaria, but the precise nature of the protective effecthas proved difficult to define as G6PD deficiency has multiple allelic variants with different effects in males and females, and it has heterogeneous effects on the clinical outcome of P. falciparum infection. Here we report an analysis of multiple allelic forms of G6PD deficiency in a large multi-centre case-control study of severe malaria, using the WHO classification of G6PD mutations to estimate each individual's level of enzyme activity from their genotype. Aggregated across all genotypes, we find that increasing levels of G6PD deficiency are associated with decreasing risk of cerebral malaria, but with increased risk of severe malarial anaemia. Models of balancing selection based on these findings indicate that an evolutionary trade-off between different clinical outcomes of P. falciparum infection could have been a major cause of the high levels of G6PD polymorphism seen in human populations.

Published
2017

41. Genome-wide and fine-resolution association analysis of malaria in West Africa

Author

Muminatou, Jallow, Yik Ying Teo, Small, Kerrin S., Rockett, Kirk A., Panos, Deloukas, Clark, Taane G., Katja, Kivinen, Bojang, Kalifa A., Conway, David J., Margaret, Pinder, Giorgio, Sirugo, Fatou Sisay Joof, Stanley, Usen, Sarah, Auburn, Bumpstead, Suzannah J., Susana, Campino, Alison, Coffey, Andrew, Dunham, Fry, Andrew E., Angela, Green, Rhian, Gwilliam, Hunt, Sarah E., Michael, Inouye, Jeffreys, Anna E., Alieu, Mendy, Aarno, Palotie, Simon, Potter, Jiannis, Ragoussis, Jane, Rogers, Kate, Rowlands, Elilan, Somaskantharajah, Pamela, Whittaker, Claire, Widden, Peter, Donnelly, Bryan, Howie, Jonathan, Marchini, Andrew, Morris, Miguel, Sanjoaquin, Eric Akum Achidi, Tsiri, Agbenyega, Angela, Allen, Olukemi, Amodu, Patrick, Corran, Abdoulaye, Djimde, Amagana, Dolo, Doumbo, Ogobara K., Chris, Drakeley, Sarah, Dunstan, Jennifer, Evans, Jeremy, Farrar, Hien Tt, Fernando D., Horstmann, R. D., Ibrahim, M., Karunaweera, N., Kokwaro, G., Koram, K. A., Lemnge, M., Makani, J., Marsh, K., Michon, P., David, Modiano, Molyneux, M. E., Mueller, I., Parker, M., Peshu, N., Plowe, C. V., Puijalon, O., Reeder, J., Reyburn, H., Riley, E. M., Sakuntabhai, A., Singhasivanon, P., Sirima, S., Tall, A., Taylor, T. E., Thera, M., Troye Blomberg, M., Williams, T. N., Wilson, M., Wellcome Trust Case Control Consortium Kwiatkowski, D. P., Epidemiology Network: Achidi, Malaria Genomic E. A., Agbenyega, T., Ahmad, T., Alcock, D., Allen, S., Amenga Etego, L., Amodu, O., Apinjoh, T. O., Attwood, A. P., Auburn, S., Ball, S. G., Balmforth, A. J., Ban, M., Barbour, J., Barnwell, D., Barrett, J. C., Barrett, J. H., Barton, A., Bentley, D., Bishop, D. T., Bojang, K., Boorman, J. P., Bougouma, E., Bradbury, L. A., Braga Marcano, C. A., Braund, P. S., Bredin, F., Breen, G., Brown, M. A., Brown, M. J., Bruce, I. N., Bryan, C., Bull, S., Bumpstead, S. J., Burke, B., Burton, P. R., Caesar, S., Campino, S., Cant, B., Cardin, N. J., Cardon, L. R., Carucci, D., Caulfield, M., Chaney, A., Clark, T., Clayton, D. G., Collier, D. A., Compston, A., Compston, D. A., Connell, J., Conway, D., Cook, K., Corran, P., Craddock, N., Cummings, F. R., Davison, D., Deloukas, P., Devries, J., Dewasurendra, R., Diakite, M., Dixon, R. J., Djimde, A., Dobson, R., Dolo, A., Dominiczak, A., Donnelly, P., Donovan, H., Doumbo, O., Downes, K., Doyle, A., Drakeley, C., Drummond, H., Duffy, P., Duncanson, A., Dunger, D. B., Dunstan, S., Duombo, O., Easton, D., Elkin, A., Elliott, K. S., Elzein, A., Enimil, A., Evans, D., Evans, J., Everson, U., Eyre, S., Farmer, A., Farrall, M., Farrar, C., Farrar, J., Fernando, D., Ferreira, T., Ferrier, I. N., Fisher, S. A., Fitzpatrick, K., Forbes, A., Franklyn, J. A., Fraser, C., Frayling, T. M., Freathy, R. M., Ghansah, A., Ghori, J., Gilbert, P. D., Gordon Smith, K., Goris, A., Gottlieb, M., Gough, S. C., Green, A., Green, E. K., Groves, C. J., Grozeva, D., Gungadoo, J., Gwilliam, R., Hall, A. S., Hallgrimsdóttir, I. B., Hamshere, M. L., Hart, L., Hattersley, A. T., Heward, J. M., Hider, S. L., Tran Tinh Hien, Hill, A. V., Hilton, E., Hinks, A. M., Hitman, G. A., Holmans, P. A., Horstmann, Rolf D., Howie, B. N., Hubbart, C., Hughes, C., Hunt, S. E., Hussein, A., Hussey, J. M., Muntaser, Ibrahim, Iles, M. M., Inouye, M., Ishengoma, D., Jallow, M., Jeffreys, A. E., Jewell, D. P., John, Sl, Jolley, J. D., Jones, I. R., Jones, L., Jones, R. W., Nadira, Karunaweera, Keniry, A., King, E., Kirov, G., Kivinen, K., Knight, A. S., Koch, K., Gilbert, Kokwaro, Koram, Kwadwo A., Lango, H., Lathrop, G. M., Lee, K. L., Lees, C. W., Martha, Lemnge, Leung, H. T., Lewis, C. M., Lin, E., Lindgren, C. M., Ly, A., Macinnis, B., Julie, Makani, Mangano, Valentina, Mangino, M., Manjurano, A., Manning, L., Mansfield, J. C., Manske, M., Maqbool, A., Marchini, J. L., Kevin, Marsh, Maslen, G., Mathew, C. G., Mcardle, W. L., Mccarthy, M. I., Mccreight, M., Mcginnis, R., Mcguffin, P., Meech, E., Mendy, A., Pascal, Michon, Mohiuddin, M. K., Molyneux, Malcolm E., Morris, A. P., Moskvina, V., Moyes, C., Ivo, Mueller, Munroe, P. B., Mutabingwa, T., Ndila, C. M., Newhouse, S. J., Newport, M., Nikolov, I., Nimmo, E. R., Nutland, S., Nyirongo, V., O'Donovan, M. C., Oluoch, T., Onipinla, A., Onnie, C. M., Ouwehand, W. H., Owen, M. J., Michael, Parker, Parkes, M., Pembrey, M., Pereira Gale, J., Perry, J. R., Norbert, Peshu, Plowe, Christopher V., Pointon, J. J., Potter, C., Potter, S., Prescott, N. J., Prowse, C. V., Odile, Puijalon, Quyen, N. T., Ragoussis, J., Rahman, N., Ravindrarajah, R., Rayner, N. W., John, Reeder, Hugh, Reyburn, Riley, Eleanor M., Ring, S. M., Risley, P., Rockett, K. A., Rogers, J., Rowlands, K., Anavaj, Sakuntabhai, Samani, N. J., Sanderson, J., Sanjoaquin, M., Satsangi, J., Sawcer, S. J., Seal, S., Shields, B. M., Silman, A. J., Simmonds, M. J., Pratap, Singhasivanon, Sodiomon, Sirima, Sirugo, G., Small, K. S., Somaskantharajah, E., Spencer, C. C., St Clair, D., Stevens, H. E., Stevens, M., Stevens, S., Strachan, D. P., Stratton, M. R., Su, Z., Suriyaphol, P., Symmons, D. P., Adama, Tall, Taylor, N. C., Taylor, Terrie E., Teo, Y., Teo, Y. Y., Mahamadou, Thera, Thompson, J. R., Thomson, W., Timpson, N. J., Tobin, M. D., Todd, J. A., Todhunter, C. E., Toure, O., Tremelling, M., Marita Troye Blomberg, Vanderwal, A., Vukcevic, D., Walker, M., Walker, N. M., Wallace, C., Walters, G. R., Walton, R., Watkins, N. A., Watson, R., Webster, J., Weedon, M. N., Whittaker, P., Widmer, B., Williams, Thomas N., Williamson, R., Michael, Wilson, Winzer, T., Withers, D., Wordsworth, P., Worthington, J., Wrigley, R., Xue, M., Young, A. H., Yuldasheva, N., and Zeggini, E.

Subjects
Linkage disequilibrium, Hemoglobin, Sickle, Population, Genome-wide association study, Locus (genetics), Biology, Population stratification, Polymorphism, Single Nucleotide, Severity of Illness Index, Linkage Disequilibrium, Article, Gene mapping, Reference Values, Ethnicity, Genetics, Humans, education, Genetic association, education.field_of_study, Polymorphism, Genetic, Chromosome Mapping, Genetic Variation, Malaria, Gambia, Imputation (genetics), Genome-Wide Association Study
Abstract

We report a genome-wide association (GWA) study of severe malaria in The Gambia. The initial GWA scan included 2,500 children genotyped on the Affymetrix 500K GeneChip, and a replication study included 3,400 children. We used this to examine the performance of GWA methods in Africa. We found considerable population stratification, and also that signals of association at known malaria resistance loci were greatly attenuated owing to weak linkage disequilibrium (LD). To investigate possible solutions to the problem of low LD, we focused on the HbS locus, sequencing this region of the genome in 62 Gambian individuals and then using these data to conduct multipoint imputation in the GWA samples. This increased the signal of association, from P = 4 × 10(-7) to P = 4 × 10(-14), with the peak of the signal located precisely at the HbS causal variant. Our findings provide proof of principle that fine-resolution multipoint imputation, based on population-specific sequencing data, can substantially boost authentic GWA signals and enable fine mapping of causal variants in African populations.

Published
2009
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43. Bednets and malaria in Africa

Author

Mathanga, D and Molyneux, M E

Subjects
Malaria -- Prevention, Insecticides -- Usage, Insect baits and repellents -- Usage, Bedding -- Care and treatment, Africa -- Health aspects
Published
2001

44. Pneumocystis carinii pneumonia in Malawian children

Author

Obaro, Steven, Graham, S M, Mtitimila, E I, Wash, A L, Hart, C A, and Molyneux, M E

Subjects
Pneumocystis carinii pneumonia -- Diagnosis, Pneumonia in children -- Diagnosis, Malawi -- Health aspects
Published
2000

48. Reappraisal of known malaria resistance loci in a large multicenter study

Author

Rockett, KA, Clarke, GM, Fitzpatrick, K, Hubbart, C, Jeffreys, AE, Rowlands, K, Craik, R, Jallow, M, Conway, DJ, Bojang, KA, Pinder, M, Usen, S, Sisay-Joof, F, Sirugo, G, Toure, O, Thera, MA, Konate, S, Sissoko, S, Niangaly, A, Poudiougou, B, Mangano, VD, Bougouma, EC, Sirima, SB, Modiano, D, Amenga-Etego, LN, Ghansah, A, Koram, KA, Wilson, MD, Enimil, A, Evans, J, Amodu, O, Olaniyan, S, Apinjoh, T, Mugri, R, Ndi, A, Ndila, CM, Uyoga, S, Macharia, A, Peshu, N, Williams, TN, Manjurano, A, Riley, E, Drakeley, C, Reyburn, H, Nyirongo, V, Kachala, D, Molyneux, M, Dunstan, SJ, Nguyen, HP, Nguyen, TNQ, Cao, QT, Tran, TH, Manning, L, Laman, M, Siba, P, Karunajeewa, H, Allen, S, Allen, A, Davis, TME, Michon, P, Mueller, I, Green, A, Molloy, S, Johnson, KJ, Kerasidou, A, Cornelius, V, Hart, L, Vanderwal, A, SanJoaquin, M, Band, G, Le, SQ, Pirinen, M, Sepulveda, N, Spencer, CCA, Clark, TG, Agbenyega, T, Achidi, E, Doumbo, O, Farrar, J, Marsh, K, Taylor, T, Kwiatkowski, DP, Rockett, KA, Clarke, GM, Fitzpatrick, K, Hubbart, C, Jeffreys, AE, Rowlands, K, Craik, R, Jallow, M, Conway, DJ, Bojang, KA, Pinder, M, Usen, S, Sisay-Joof, F, Sirugo, G, Toure, O, Thera, MA, Konate, S, Sissoko, S, Niangaly, A, Poudiougou, B, Mangano, VD, Bougouma, EC, Sirima, SB, Modiano, D, Amenga-Etego, LN, Ghansah, A, Koram, KA, Wilson, MD, Enimil, A, Evans, J, Amodu, O, Olaniyan, S, Apinjoh, T, Mugri, R, Ndi, A, Ndila, CM, Uyoga, S, Macharia, A, Peshu, N, Williams, TN, Manjurano, A, Riley, E, Drakeley, C, Reyburn, H, Nyirongo, V, Kachala, D, Molyneux, M, Dunstan, SJ, Nguyen, HP, Nguyen, TNQ, Cao, QT, Tran, TH, Manning, L, Laman, M, Siba, P, Karunajeewa, H, Allen, S, Allen, A, Davis, TME, Michon, P, Mueller, I, Green, A, Molloy, S, Johnson, KJ, Kerasidou, A, Cornelius, V, Hart, L, Vanderwal, A, SanJoaquin, M, Band, G, Le, SQ, Pirinen, M, Sepulveda, N, Spencer, CCA, Clark, TG, Agbenyega, T, Achidi, E, Doumbo, O, Farrar, J, Marsh, K, Taylor, T, and Kwiatkowski, DP

Abstract

Many human genetic associations with resistance to malaria have been reported, but few have been reliably replicated. We collected data on 11,890 cases of severe malaria due to Plasmodium falciparum and 17,441 controls from 12 locations in Africa, Asia and Oceania. We tested 55 SNPs in 27 loci previously reported to associate with severe malaria. There was evidence of association at P < 1 × 10(-4) with the HBB, ABO, ATP2B4, G6PD and CD40LG loci, but previously reported associations at 22 other loci did not replicate in the multicenter analysis. The large sample size made it possible to identify authentic genetic effects that are heterogeneous across populations or phenotypes, with a striking example being the main African form of G6PD deficiency, which reduced the risk of cerebral malaria but increased the risk of severe malarial anemia. The finding that G6PD deficiency has opposing effects on different fatal complications of P. falciparum infection indicates that the evolutionary origins of this common human genetic disorder are more complex than previously supposed.

Published
2014

50. Mutations Associated with Sulfadoxine-Pyrimethamine and Chlorproguanil Resistance in Plasmodium falciparum Isolates from Blantyre, Malawi

Author

Kamwendo, D. D., Purfield, A., Rogerson, S. J., Molyneux, M. E., Meshnick, S. R., Mwapasa, V., Alker, A. P., Chaluluka, E., and Tadesse, E.

Subjects
parasitic diseases, humanities
Abstract

We conducted a prevalence study of mutations in Plasmodium falciparum that are associated with antifolate resistance in Blantyre, Malawi. The dihydrofolate reductase 164-Leu mutation, which confers resistance to both pyrimethamine and chlorproguanil, was found in 4.7% of the samples. Previously unreported mutations in dihydropteroate synthase were also found.

Published
2005
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