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      Insecticide resistance in mosquitoes: impact, mechanisms, and research directions.

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          Abstract

          Mosquito-borne diseases, the most well known of which is malaria, are among the leading causes of human deaths worldwide. Vector control is a very important part of the global strategy for management of mosquito-associated diseases, and insecticide application is the most important component in this effort. However, mosquito-borne diseases are now resurgent, largely because of the insecticide resistance that has developed in mosquito vectors and the drug resistance of pathogens. A large number of studies have shown that multiple, complex resistance mechanisms-in particular, increased metabolic detoxification of insecticides and decreased sensitivity of the target proteins-or genes are likely responsible for insecticide resistance. Gene overexpression and amplification, and mutations in protein-coding-gene regions, have frequently been implicated as well. However, no comprehensive understanding of the resistance mechanisms or regulation involved has yet been developed. This article reviews current knowledge of the molecular mechanisms, genes, gene interactions, and gene regulation governing the development of insecticide resistance in mosquitoes and discusses the potential impact of the latest research findings on the basic and practical aspects of mosquito resistance research.

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          Author and article information

          Journal
          Annu. Rev. Entomol.
          Annual review of entomology
          1545-4487
          0066-4170
          Jan 7 2015
          : 60
          Affiliations
          [1 ] Department of Entomology and Plant Pathology, Insect Molecular Toxicology and Physiology Program, Auburn University, Auburn, Alabama 36849; email: liunann@auburn.edu.
          Article
          10.1146/annurev-ento-010814-020828
          25564745
          7272d8c0-a488-4d56-aa1c-f29558ff9d1a
          History

          functional study,insecticide resistance,metabolic detoxification,resistance-gene regulation,target-site insensitivity

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