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Volumn 287, Issue 5454, 2000, Pages 845-848

Cross-species interactions between malaria parasites in humans

Author keywords

[No Author keywords available]

Indexed keywords

ARTICLE; DISEASE TRANSMISSION; GENOTYPE; HUMAN; IMMUNE RESPONSE; INFECTION RISK; MALARIA; PLASMODIUM; PRIORITY JOURNAL; SPECIES DIFFERENCE;

EID: 0034602943     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.287.5454.845     Document Type: Article
Times cited : (187)

References (36)
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    • note
    • This study was carried out in the village of Gonoa, Madang Province, Papua New Guinea, between 28 June and 27 August 1992 (15). Children ≥4 years old were enrolled following informed consent from parents or guardians. Clinical malaria and drug use was monitored by self-reporting. One child reporting fever was eliminated from the study. Only children with ≥50% compliance with sampling were used in analyses. Ethical clearance was granted by the Medical Research Advisory Committee of Papua New Guinea, who recommend that asymptomatic malaria infections should not be treated in order to allow natural, protective immunity to develop.
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    • Parasite species density was obtained from thick and thin blood smears. Smears were air-dried, thin smears were fixed in methanol, and both were stained in 4% Giemsa in sodium phosphate buffer (pH 7.2) for 45 min. Enumeration was per 200 leukocytes and counts were converted to parasites/μl of blood, assuming 8000 leukocytes/μl.
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    • All samples were analyzed from children with ≥2 P. falciparum smear-positive samples or ≥4 F. vivax positives (15). Blood from finger pricks was collected in EDTA and stored at -70°C, then 20-μl volumes were transferred to filter paper for DNA extraction [S. Kyes, A. G. Craig, K. Marsh, C. I. Newbold, Exp. Parasitol. 77, 473 (1993)]. Plasmodium falciparum genotypes were determined by size and sequence polymorphisms in PCR-amplified alleles of the merozoite surface protein 2 (Msp2) gene [H. Babiker, L. Ranford-Cartwright, A. Sultan, G. Satti, D. Walliker, Trans. R. Soc. Trop. Med. Hyg. 88, 328 (1994)]. Plasmodium vivax genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis [M. C. Bruce, M. R. Galinski, J. W. Barnwell, G. Snouou, K. P. Day, Am. J. Trop. Med. Hyg. 61, 518 (1999)] of alleles at the merozoite surface protein 3 alpha (Msp3α) locus [M. R. Galinski et al., Mol. Biochem. Parasitol. 101, 131 (1999)].
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    • All samples were analyzed from children with ≥2 P. falciparum smear-positive samples or ≥4 F. vivax positives (15). Blood from finger pricks was collected in EDTA and stored at -70°C, then 20-μl volumes were transferred to filter paper for DNA extraction [S. Kyes, A. G. Craig, K. Marsh, C. I. Newbold, Exp. Parasitol. 77, 473 (1993)]. Plasmodium falciparum genotypes were determined by size and sequence polymorphisms in PCR-amplified alleles of the merozoite surface protein 2 (Msp2) gene [H. Babiker, L. Ranford-Cartwright, A. Sultan, G. Satti, D. Walliker, Trans. R. Soc. Trop. Med. Hyg. 88, 328 (1994)]. Plasmodium vivax genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis [M. C. Bruce, M. R. Galinski, J. W. Barnwell, G. Snouou, K. P. Day, Am. J. Trop. Med. Hyg. 61, 518 (1999)] of alleles at the merozoite surface protein 3 alpha (Msp3α) locus [M. R. Galinski et al., Mol. Biochem. Parasitol. 101, 131 (1999)].
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    • All samples were analyzed from children with ≥2 P. falciparum smear-positive samples or ≥4 F. vivax positives (15). Blood from finger pricks was collected in EDTA and stored at -70°C, then 20-μl volumes were transferred to filter paper for DNA extraction [S. Kyes, A. G. Craig, K. Marsh, C. I. Newbold, Exp. Parasitol. 77, 473 (1993)]. Plasmodium falciparum genotypes were determined by size and sequence polymorphisms in PCR-amplified alleles of the merozoite surface protein 2 (Msp2) gene [H. Babiker, L. Ranford-Cartwright, A. Sultan, G. Satti, D. Walliker, Trans. R. Soc. Trop. Med. Hyg. 88, 328 (1994)]. Plasmodium vivax genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis [M. C. Bruce, M. R. Galinski, J. W. Barnwell, G. Snouou, K. P. Day, Am. J. Trop. Med. Hyg. 61, 518 (1999)] of alleles at the merozoite surface protein 3 alpha (Msp3α) locus [M. R. Galinski et al., Mol. Biochem. Parasitol. 101, 131 (1999)].
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    • All samples were analyzed from children with ≥2 P. falciparum smear-positive samples or ≥4 F. vivax positives (15). Blood from finger pricks was collected in EDTA and stored at -70°C, then 20-μl volumes were transferred to filter paper for DNA extraction [S. Kyes, A. G. Craig, K. Marsh, C. I. Newbold, Exp. Parasitol. 77, 473 (1993)]. Plasmodium falciparum genotypes were determined by size and sequence polymorphisms in PCR-amplified alleles of the merozoite surface protein 2 (Msp2) gene [H. Babiker, L. Ranford-Cartwright, A. Sultan, G. Satti, D. Walliker, Trans. R. Soc. Trop. Med. Hyg. 88, 328 (1994)]. Plasmodium vivax genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis [M. C. Bruce, M. R. Galinski, J. W. Barnwell, G. Snouou, K. P. Day, Am. J. Trop. Med. Hyg. 61, 518 (1999)] of alleles at the merozoite surface protein 3 alpha (Msp3α) locus [M. R. Galinski et al., Mol. Biochem. Parasitol. 101, 131 (1999)].
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    • note
    • We thank the people of Gonoa for their long-standing cooperation and the staff of the Papua New Guinea Institute of Medical Research, Madang, for their assistance. Supported by grants to K.P.D., D.W., and M.P.A. from the European Commission, by a grant to K.P.D. from the Wellcome Trust, by NIH grant AI24710 to J.W.B., and NIH grant AI37545 and World Health Organization/TDR grants (950440 and 910495) to M.R.G. M.C.B. was supported by The UK Medical Research Council and The Wellcome Trust. C.A.D. was supported by The Wellcome Trust.


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