Larval Competition Extends Developmental Time and Decreases Adult Size of wMelPop Wolbachia-Infected Aedes aegypti

Perran A. Ross Bio21 Institute and Department of Genetics, University of Melbourne, Melbourne, Victoria, Australia

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Nancy M. Endersby Bio21 Institute and Department of Genetics, University of Melbourne, Melbourne, Victoria, Australia

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Heng Lin Yeap Bio21 Institute and Department of Genetics, University of Melbourne, Melbourne, Victoria, Australia

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Ary A. Hoffmann Bio21 Institute and Department of Genetics, University of Melbourne, Melbourne, Victoria, Australia

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The intracellular endosymbiont Wolbachia has been artificially transinfected into the dengue vector Aedes aegypti, where it is being investigated as a potential dengue biological control agent. Invasion of Wolbachia in natural populations depends upon the fitness of Wolbachia-infected Ae. aegypti relative to uninfected competitors. Although Wolbachia infections impose fitness costs on the adult host, effects at the immature stages are less clear, particularly in competitive situations. We look for effects of two Wolbachia infections, wMel and wMelPop, on intra-strain and inter-strain larval competition in Ae. aegypti. Development of Wolbachia-infected larvae is delayed in mixed cohorts with uninfected larvae under crowded-rearing conditions. Slow developing wMelPop-infected larvae have reduced adult size compared with uninfected larvae, and larvae with the wMel infection are somewhat larger and have greater viability relative to uninfected larvae when in mixed cohorts. Implications for successful invasion by these Wolbachia infections under field conditions are considered.

Author Notes

* Address correspondence to Perran A. Ross, Pest and Disease Vector Group, Bio21 Institute and the Department of Genetics, University of Melbourne, Parkville, VIC 3052, Australia. E-mail: paross@student.unimelb.edu.au

Financial support: This study was supported by the National Health and Medical Research Council. Ary A. Hoffmann was supported by Laureate Fellowship from the Australian Research Council.

Authors' addresses: Perran A. Ross, Nancy M. Endersby, Heng Lin Yeap, and Ary A. Hoffmann, Pest and Disease Vector Group, Bio21 Institute and the Department of Genetics, University of Melbourne, Parkville, Australia, E-mails: paross@student.unimelb.edu.au, nancye@unimelb.edu.au, hlyeap@unimelb.edu.au, and ary@unimelb.edu.au.

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