Aedes aegypti is the most important arboviral disease vector worldwide. In Africa, it exists as two morphologically distinct forms, often referred to as subspecies, Aaa and Aaf. There is a dearth of information on the distribution and genetic diversity of these two forms in Sudan and other African Sahelian region countries. This study aimed to explore the distribution and genetic diversity of Aedes aegypti subspecies using morphology and Cytochrome oxidase-1 mitochondrial marker in a large Sahelian zone in Sudan. An extensive cross-sectional survey of Aedes aegypti in Sudan was performed. Samples collected from eight locations were morphologically identified, subjected to DNA extraction, amplification, sequencing, and analyses. We classified four populations as Aaa and the other four as Aaf. Out of 140 sequence samples, forty-six distinct haplotypes were characterized. The haplotype and nucleotide diversity of the collected samples were 0.377–0.947 and 0.002–0.01, respectively. Isolation by distance was significantly evident (r = 0.586, p = 0.005). The SAMOVA test indicated that all Aaf populations are structured in one group, while the Aaa clustered into two groups. AMOVA showed 53.53% genetic differences within populations and 39.22% among groups. Phylogenetic relationships indicated two clusters in which the two subspecies were structured. Thus, the haplotype network consisted of three clusters.
Mosquito coils are insecticides commonly used for protection against mosquitoes due to their toxic effects on mosquito populations. These effects on mosquitoes could induce the expression of metabolic enzymes in exposed populations as a counteractive measure. Cytochrome P450 family 4 (CYP4) are metabolic enzymes associated with a wide range of biological activities including insecticide resistance. In this study, the efficacies of three commercial mosquito coils with different pyrethroid active ingredients were assessed and their potential to induce the expression of CYP4 genes in Aedes albopictus analyzed by real-time quantitative PCR. Coils containing 0.3 % D-allethrin and 0.005 % metofluthrin exacted profound toxic effects on Ae. albopictus, inducing high mortalities (≥90 %) compared to the 0.2 % D-allethrin reference coil. CYP4H42 and CYP4H43 expressions were significantly higher in 0.3 % D-allethrin treated mosquitoes compared to the other treated populations. Short-term (KT50) exposure to mosquito coils induced significantly higher expression of both genes in 0.005 % metofluthrin exposed mosquitoes. These results suggest the evaluated products provided better protection than the reference coil; however, they also induced the expression of metabolic genes which could impact negatively on personal protection against mosquito.
Although evidence of mosquito coils' impact on disease epidemiology is limited, they are popularized as mosquito-borne disease prevention devices. Their usage affects the environment, human and mosquito health. This study investigated the perception, usage pattern and efficacy of coils in a predominantly poor malaria-endemic Ghanaian peri-urban area. Information on protection methods, perception and usage pattern was garnered using questionnaires. The efficacy of commonly used coils in the area was then assessed on the malaria vector, Anopheles gambiae, in a glass chamber. Sole or co-application of mosquito control methods and risky usage practices were reported. Coils were deemed harmful to humans and mosquitoes, and their perceived effectiveness varied, with several factors influencing their purchase. High d-allethrin concentration coils induced quicker mosquito knockdown; however, mortality was less than 85%. The coil usage pattern compromises users' health and can enhance mosquito tolerance to d-allethrin. The coils were ineffective against the vector, outlining a dichotomy between the users' perception of efficacy and the observed efficacy. Hence, the usage of other safer and more effective vector control methods should be encouraged to protect households.
Mammalian cytochrome P450s provide our first line of defence against the toxic effects of environmental chemicals. Ironically these enzymes also convert some compounds to their ultimate toxic or mutagenic species. Our knowledge of these mammalian enzymes and the role they play in chemical toxicity and mutagenesis has stemmed mostly from in vitro studies. In order to establish the role of specific enzymes in the toxicological response in vivo we have generated transgenic Drosophila which express mammalian cytochrome CYP2B1, which is a member of a large gene family encoding several important drug metabolising enzymes. The gene was fused to a Drosophila promoter which confers expression in the larval fat body. Using the Somatic Mutation And Recombination Test (SMART) we have demonstrated that transgenic larvae expressing the P450 are hypersensitive to the anticancer drug cyclophosphamide, a procarcinogenic substrate which is activated by the enzyme. This work demonstrates the potential of such transgenic Drosophila strains as an in vivo model for studying the role of specific mammalian drug metabolising enzymes in the pathways and metabolic cascades associated with the action of cytotoxic and carcinogenic chemicals, and also the chemical properties of specific classes of mutagen to be determined.
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