Evolution of phenotypic and molecular insecticide resistance in malaria vectors in Burkina Faso (2016-2025): A systematic review and quantitative synthesis

Insecticide-based vector control remains central to malaria prevention in Burkina Faso, but its effectiveness is increasingly threatened by intense and multi-mechanistic resistance in malaria vectors. This review synthesizes evidence generated between 2016 and 2025 on phenotypic resistance, resistance intensity, molecular markers, metabolic mechanisms and emerging genomic signatures in Anopheles populations from Burkina Faso. A systematic review and quantitative synthesis were conducted following PRISMA principles. Eligible sources reported insecticide susceptibility bioassays, resistance-intensity assays, synergist assays, target-site mutations, metabolic indicators or genomic resistance markers in malaria vectors from Burkina Faso. Because studies differed in design, insecticide panels, vector species and reporting formats, findings were summarized through structured quantitative synthesis rather than formal pooled meta-analysis. The final evidence base included 73 studies or reports, including 29 records with detailed structured extraction and 42 usable pyrethroid mortality estimates. Pyrethroid resistance was consistently reported across Sahelian, Sudano-Sahelian and Sudanian settings. In the broadest sentinel survey, mean mortality in Anopheles gambiae s.l. was 33.2% for deltamethrin, 24.5% for permethrin and 19.0% for alpha-cypermethrin. Resistance intensity was frequently high. Vgsc-L1014F/L995F and Vgsc-L1014S/L995S were widespread but heterogeneous, while genomic evidence indicated diversification through additional VGSC variants, ace-1/ace1 signals and copy-number variation in detoxification gene families. PBO synergist assays often increased pyrethroid mortality but rarely restored full susceptibility, indicating multifactorial resistance. Chlorfenapyr susceptibility was largely retained where tested. Between 2016 and 2025, malaria vectors in Burkina Faso shifted from widespread pyrethroid resistance toward more complex resistance systems combining target-site, metabolic and genomic mechanisms. Resistance management should prioritize mechanism-aware surveillance, chlorfenapyr-based dual-active-ingredient nets in high-resistance areas, targeted PBO-net deployment and preservation of organophosphate susceptibility through rotation and genomic monitoring.