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Genetic Mapping of the Duffy Binding Protein (DBP) Ligand Domain of Plasmodium vivax from Unstable Malaria Region in the Middle East

The region II of Plasmodium vivax Duffy binding protein (PvDBP–II) contains the critical binding residues, which is a major target for development of naturally acquired immunity. Several studies showed sequence polymorphisms in PvDBP–II, which may inhibit antibodies recognition. Therefore, in this study the level of PvDBP–II polymorphism within and among P. vivax populations from re-emerged areas in north and endemic areas in south of Iran were evaluated by sequencing analysis in 75 isolates for the first time. Fourteen non-synonymous and one synonymous mutations were identified and none of the amino acid substitutions were directly involved in erythrocyte binding. Only 6 out of 14 detected mutations have been found among northern isolates, including D384G, R390H, N417K, L424I, W437R, and I503K. In total, two and nine different variants have been identified among northern and southern isolates, respectively. High association of the amino acid frequencies for codons 417, 437, and 503 were found among northern (85% for trio association and 100% for N417K with W437R), and southern (36% for trio association and 98% for N417K with W437R) samples. Polymorphisms at positions R308S, K371E, D384G, K386N, R390H, N417K, L424I, W437R, and I503K were identified from Iran and diverse geographic areas; however, mutation at position F306L was only reported from Asian malaria endemic areas. It is suggested that to develop polyvalent vaccine against P. vivax infection, it is better to incorporate the common and high prevalent allelic variants of the antigen that were reported from different malaria endemic regions.

Received May 12, 2008. Accepted for publication September 19, 2008.

Acknowledgments: We thank the Malaria Division, CDC, Iran, for their cooperation. We are grateful for the hospitality and generous collaboration of Zahedan University of Medical Sciences, and the staff of the Public Health Department, Sistan and Baluchistan province, Chabahar district (Dr. Mehdizadeh, and Mr. Gorgij), and Pars–Abad, Ardebil (Dr. Arshi, Mr. Emdadi) for their assistance in collecting blood samples from the field. We also express our sincere thanks to the patients in Chabahar and Pars–Abad, for their participation in this study.

Financial support: This work was financially supported through research grant No. 264 from Pasteur Institute of Iran to S. Zakeri.

^* Address correspondence to Sedigheh Zakeri, Malaria Research Group (MRG), Biotechnology Department, Pasteur Institute of iran, Pasteur Avenue, P.O. Box 1316943551, Tehran, Iran. E-mail: zakeris{at}pasteur.ac.ir

Authors’ addresses: Laleh Babaeekho, Science and Research Branch, Islamic Azad University, Tehran, Iran. Sedigheh Zakeri and Navid Dinparast Djadid, Malaria and Vector Research Group (MVRG), Biotechnology Research Center, Pasteur Institute of Iran, Pasteur Avenue, P.O. Box 1316943551, Tehran, Iran, Tel: 98-21-66480780, Fax: 98-21-66465132.

Reprint requests: Sedigheh Zakeri, Malaria and Vector Research Group (MVRG), Biotechnlogy Research Centre, Pasteur Institute of Iran, Tehran, Iran, E-mail: zakeris{at}pasteur.ac.ir.