The evolution of pyrethroid insecticide resistance in Culex tarsalis Coquillett, a vector for West Nile and St. Louis encephalitis viruses, is a growing concern in Northern California. Common mechanisms of resistance include the target-site mutation, kdr, and increased levels of detoxification enzymes, such as mixed-function oxidases, GSTs, and esterases. The goal of this study was to compare the prevalence of kdr mutations (L1014F and L1014S) and detoxification enzymes between pyrethroid susceptible and resistant Cx. tarsalis individuals. Individual mosquitoes, categorized by resistance status from permethrin bottle bioassays, were prepared for both molecular and enzymatic testing by separating the legs of a mosquito from the remaining body. Legs were used to test for the presence of kdr mutations, while the bodies were used to test for the activity of detoxification enzymes. The number of phenylalanine (F) alleles present at the kdr target-site as well as levels of GST were increased in mosquitoes that survived the bottle bioassay compared to those that were knocked down. Individuals with 2 F alleles and an active GST level greater than or equal to 0.052 µg/ml showed a higher survival rate than either mechanism independently demonstrating resistance to pyrethroids in Cx. tarsalis is likely the result of multiple resistance mechanisms acting collectively. Further work is needed to determine the interplay of multiple resistance mechanisms to achieve phenotype resistance in this mosquito species.
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http://dx.doi.org/10.1093/jme/tjaf001 | DOI Listing |
Langmuir
March 2025
Jiangxi Province Key Laboratory of Light Alloy, School of Advanced Manufacturing, Nanchang University, Nanchang 330031, P.R. China.
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Laboratory of Histology and Embryology, Aristotle University Medical School, Thessaloniki, Greece.
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Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, P. R. China.
The von Hippel-Lindau (VHL) tumor suppressor gene VHL is a classic tumor suppressor that has been identified in family members with clear cell renal cell carcinomas, central nervous system and retinal hemangioblastomas, phaeochromocytomas, and pancreatic neuroendocrine tumors. The well-defined function of VHL is to mediate proteasomal degradation of hydroxylated hypoxia-inducible factor α proteins, resulting in the downregulation of hypoxia-responsive gene expression. Previously, we reported that VHL inhibits antiviral signaling by targeting mitochondrial antiviral signaling protein (MAVS) for proteasomal degradation.
View Article and Find Full Text PDFJ Immunol
January 2025
Division of Oncology, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO, United States.
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View Article and Find Full Text PDFJ Immunol
March 2025
School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104 United States.
Interleukin 33 (IL-33) is a pleiotropic cytokine released from diverse cell types that regulate both pro- and anti-inflammatory responses during pathogen infection. However, it remains unclear whether IL-33 controls key aspects of cutaneous immunity against skin-penetrating parasites. In this study, mice percutaneously infected with the parasitic helminth Strongyloides ratti were investigated to understand mechanisms of anamnestic immunity at the skin barrier.
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