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Am. J. Trop. Med. Hyg., 73(2), 2005, pp. 445-449
Copyright © 2005 by The American Society of Tropical Medicine and Hygiene

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POTENTIAL ROLE OF SYLVATIC AND DOMESTIC AFRICAN MOSQUITO SPECIES IN DENGUE EMERGENCE

MAWLOUTH DIALLO, AMADOU A. SALL, ABELARDO C. MONCAYO, YAMAR BA, ZORAIDA FERNANDEZ, DIANA ORTIZ, LARK L. COFFEY, CHRISTIAN MATHIOT, ROBERT B. TESH, AND SCOTT C. WEAVER*
Institut Pasteur de Dakar, Dakar, Senegal; Center for Biodefense and Emerging Infectious Diseases and Department of Pathology, University of Texas Medical Branch, Galveston, Texas

Dengue virus 2 (DENV-2) strains that circulate in sylvatic habitats of Senegal and other parts of west Africa are believed to represent ancestral forms that evolved into endemic/epidemic strains that now circulate widely in urban areas of the tropics. Previous studies suggested that the evolution of the endemic/epidemic strains was mediated by adaptation to the peridomestic mosquito vectors Aedes aegypti and Ae. albopictus. We conducted experimental infections using sylvatic and peridomestic Senegalese mosquitoes, and both sylvatic and urban DENV-2 strains to determine if endemic DENV-2 adaptation was vector species specific, and to assess ancestral vector susceptibility. Aedes furcifer and Ae. luteocephalus, probable sylvatic vectors, were highly susceptible to both sylvatic and urban DENV-2 strains. In contrast, sylvatic Ae. vittatus and both sylvatic and peridomestic populations of Ae. aegypti were relative refractory to all DENV-2 strains tested. These results indicate that adaptation of DENV-2 to urban vectors did not result in a loss of infectivity for some African sylvatic vectors. Implications for dengue emergence in west Africa are discussed.


Received October 25, 2004. Accepted for publication April 8, 2005.

Acknowledgment: We thank Wenli Kang for excellent technical assistance.

Financial support: This work was supported by grants TW01162, AI10984, and AI39800 from the National Institutes of Health. Lark L. Coffey was supported by the James W. McLaughlin Fellowship fund.

* Address correspondence to Dr. Scott C. Weaver, Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609. E-mail: sweaver{at}utmb.edu.

Authors’ addresses: Mawlouth Diallo, Amadou A. Sall, and Yamar Ba, Institut Pasteur de Dakar, 36 Avenue Pasteur Dakar, Senegal, E-mails: diallo{at}pasteur.sn, asall{at}pasteur.sn, and ba{at}pasteur.sn. Abelardo C. Moncayo, Tennessee Department of Health, Communicable and Environmental Services, Cordell Hull Building, 425 Fifth Avenue North, Nashville, TN 37247-4911, E-mail: a-moncayo{at}onu.edu. Zoraida Fernandez, Instituto Venezolano de Investigaciones Cientificas, Carretera Panamericana Km 11, Altos de Pipe, Apartado Postal 1040-A, Caracas, Venezuela, Fax: 0212-5041489, E-mail: zofernam{at}hotmail.com. Diana Ortiz, Lark L. Coffey, Robert B. Tesh, and Scott C. Weaver, Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609, Fax: 409-747-2415, E-mails: diortiz{at}hotmail.com, llcoffey{at}utmb.edu, rtesh{at}utmb.edu, and sweaver{at}utmb.edu. Christian Mathiot, World Health Organization, 58 Avenue Debourg, 69007 Lyon, France, Fax: 33-4-72-71-64-71, E-mail: mathiotc{at}lyon.who.int.

Reprint requests: Scott C. Weaver, Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609.




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[Abstract] [Full Text] [PDF]




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