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Anopheles darlingi is the most important malaria vector in the Amazon basin of South America, and is capable of transmitting both Plasmodium falciparum and P. vivax. To understand the genetic structure of this vector in the Amazonian region of Peru, a simple polymerase chain reaction (PCR)–based test to identify this species of mosquito was used. A random amplified polymorphic DNA–PCR was used to study genetic variation at the micro-geographic level in nine geographically separate populations of An. darlingi collected in areas with different degrees of deforestation surrounding the city of Iquitos. Within-population genetic diversity in nine populations, as quantified by the expected heterozygosity (HE), ranged from 0.27 to 0.32. Average genetic distance (FST) among these populations was 0.017. These results show that the nine studied populations are highly homogeneous, suggesting that strategies can be developed to combat this malaria vector as a single epidemiologic unit.
Received December 14, 2005. Accepted for publication March 10, 2006.
Acknowledgments: We appreciate the helpful work of Drs. Jan E. Conn (Wadsworth Center, New York State Department of Health, Slingerlands, NY) and Ranulfo Gonzáles (Department of Biology, Valle University, Cali, Colombia). We also thank Dr. Gregory J. Devine (Rothamsted Research, Harpenden, United Kingdom) for his helpful comments and Lizardo Fachin (Unidad de Información Geográfica y Teledetección-IIAP, Iquitos) for designing the map. We are grateful to numerous collaborators for assistance in collecting samples for this research, particularly the field team in Peru.
Financial support: This study was supported by the Doris Duke Charitable Foundation, Infectious Diseases Training Program, Charitable RG-ER funds (3D43TW006581); and the Fogarty Global Research and Tutorial in Tropical Health at Johns Hopkins University/Peru Overseas (T35AI07646 National Institutes of Health/National Institute of Allergy and Infectious Diseases).
Disclaimer: The opinions and assertions made by the authors do not reflect the official position of any organization listed.
Disclosure: All authors declare that they have no conflict of interest in relation to this work.
* Address correspondence to Robert H. Gilman, Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Room 5515, Baltimore, MD 21205. E-mail: rgilman{at}jhsph.edu
Authors’ addresses: Viviana Vanessa Pinedo-Cancino, Patricia Sheen, and Cesar Jeri, Laboratory of Infectious Diseases, Department of Microbiology, Faculty of Sciences, Peruvian University Cayetano Heredia, Lima, Peru Avenida Honorio Delgado No. 430 Urbanización Ingeniería, San Martín de Porras, Peru, Telephone: 1-483-2942, Fax: 1-483-2942. Eduardo Tarazona-Santos, Section of Genomic Variation, Pediatric Oncology Branch, National Cancer Institute; Department of General Biology, Federal University of Minas Gerais, Belo Horizonte, Brazil Av. Antônio Carlos, 6627, Caixa-Postal: 486 Pampulha, 31270910, Belo Horizonte, Minas Gerais, Brazil. William E. Oswald, Biomedical Research Unit, Asociación Benéfica PRISMA (Projects in Informatics, Health, Medicine and Agriculture), Lima, Peru Avenida Carlos Gonzales 251, Urbanización Maranga, San Miguel, Peru, Telephone: 1-464-0221, Fax: 1-464-0781. Amy Yomiko Vittor, School of Medicine, Stanford University, Stanford, CA 94305. Jonathan A. Patz, Nelson Institute for Environmental Studies, University of Wisconsin, 1710 University Avenue, Madison, WI 53726, Telephone: 608-262-4775, Fax: 608-265-4113. Robert H. Gilman, Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Room 5515, Baltimore, MD 21205, Telephone: 410-614-3959, E-mail: rgilman{at}jhsph.edu.
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