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Analyzing the control of mosquito-borne diseases by a dominant lethal genetic system.

ABSTRACT: Motivated by the failure of current methods to control dengue fever, we formulate a mathematical model to assess the impact on the spread of a mosquito-borne viral disease of a strategy that releases adult male insects homozygous for a dominant, repressible, lethal genetic trait. A dynamic model for the female adult mosquito population, which incorporates the competition for female mating between released mosquitoes and wild mosquitoes, density-dependent competition during the larval stage, and realization of the lethal trait either before or after the larval stage, is embedded into a susceptible-exposed-infectious-susceptible human-vector epidemic model for the spread of the disease. For the special case in which the number of released mosquitoes is maintained in a fixed proportion to the number of adult female mosquitoes at each point in time, we derive mathematical formulas for the disease eradication condition and the approximate number of released mosquitoes necessary for eradication. Numerical results using data for dengue fever suggest that the proportional policy outperforms a release policy in which the released mosquito population is held constant, and that eradication in approximately 1 year is feasible for affected human populations on the order of 10(5) to 10(6), although the logistical considerations are daunting. We also construct a policy that achieves an exponential decay in the female mosquito population; this policy releases approximately the same number of mosquitoes as the proportional policy but achieves eradication nearly twice as fast.

SUBMITTER: Atkinson MP

PROVIDER: S-EPMC1876161 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Many of the world's most prevalent diseases are transmitted by animal vectors such as dengue transmitted by mosquitoes. To reduce these vector-borne diseases, a promising approach is "genetic shifting": selective breeding of the vectors to be more resistant to pathogens and releasing them to the target populations to reduce their ability to transmit pathogens, that is, lower their vector competence. The efficacy of genetic shifting will depend on possible counterforces such as natural selection against low vector competence. To quantitatively evaluate the potential efficacy of genetic shifting, we developed a series of coupled genetic-demographic models that simulate the changes of vector competence during releases of individuals with low vector competence. We modeled vector competence using different genetic architectures, as a multilocus, one-locus, or two-locus trait. Using empirically determined estimates of model parameters, the model predicted a reduction of mean vector competence of at least three standard deviations after 20 releases, one release per generation, and 10% of the size of the target population released each time. Sensitivity analysis suggested that release efficacy depends mostly on the vector competence of the released population, release size, release frequency, and the survivorship of the released individuals, with duration of the release program less important. Natural processes such as density-dependent survival and immigration from external populations also strongly influence release efficacy. Among different sex-dependent release strategies, releasing blood-fed females together with males resulted in the highest release efficacy, as these females mate in captivity and reproduce when released, thus contributing a greater proportion of low-vector-competence offspring. Conclusions were generally consistent across three models assuming different genetic architectures of vector competence, suggesting that genetic shifting could generally apply to various vector systems and does not require detailed knowledge of the number of loci contributing to vector competence.

Project description:Malaria, dengue fever, and filariasis are three of the most common mosquito-borne diseases worldwide. Malaria and lymphatic filariasis can occur as concomitant human infections while also sharing common mosquito vectors. The overall prevalence and health significance of malaria and filariasis have made them top priorities for global elimination and control programmes. Pyrethroid resistance in anopheline mosquito vectors represents a highly significant problem to malaria control worldwide. Several methods have been proposed to mitigate insecticide resistance, including rotational use of insecticides with different modes of action. Anopheles sinensis, an important malaria and filariasis vector in Southeast Asia, represents an interesting mosquito species for examining the consequences of long-term insecticide rotation use on resistance. We examined insecticide resistance in two An. Sinensis populations from central and southern China against pyrethroids, organochlorines, organophosphates, and carbamates, which are the major classes of insecticides recommended for indoor residual spray. We found that the mosquito populations were highly resistant to the four classes of insecticides. High frequency of kdr mutation was revealed in the central population, whereas no kdr mutation was detected in the southern population. The frequency of G119S mutation in the ace-1 gene was moderate in both populations. The classification and regression trees (CART) statistical analysis found that metabolic detoxification was the most important resistance mechanism, whereas target site insensitivity of L1014 kdr mutation played a less important role. Our results indicate that metabolic detoxification was the dominant mechanism of resistance compared to target site insensitivity, and suggests that long-term rotational use of various insecticides has led An. sinensis to evolve a high insecticide resistance. This study highlights the complex network of mechanisms conferring multiple resistances to chemical insecticides in mosquito vectors and it has important implication for designing and implementing vector resistance management strategies.

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Analyzing the control of mosquito-borne diseases by a dominant lethal genetic system.

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