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Background  In recent years, the scale-up of long-lasting insecticidal nets (LLINs) and indoor residual spraying (IRS) has greatly reduced malaria transmission. However, malaria remains a global public health concern with the majority of the disease burden in sub-Saharan Africa. Insecticide resistance is a growing problem among  Anopheles  vector populations, with potential implications for the continued effectiveness of available control interventions. Improved understanding of current resistance levels and underlying mechanisms is essential to design appropriate management strategies and to mitigate future selection for resistance.    Methods   Anopheles gambiae  sensu lato mosquitoes were collected from three villages in Faranah Prefecture, Guinea and their levels of susceptibility to seven insecticides were measured using CDC resistance intensity bioassays. Synergist assays with piperonyl butoxide (PBO) were also undertaken to assess the role of elevated mixed-function oxidases in resistance. Five hundred and sixty-three mosquitoes underwent molecular characterization of vector species, presence of target site mutations (L1014F  kdr , N1575Y and G119S  Ace - 1 ),  Plasmodium falciparum  infection, and relative expression of three metabolic genes ( CYP6M2 ,  CYP6P3  and  GSTD3 ).    Results  In Faranah, resistance to permethrin and deltamethrin was observed, as well as possible resistance to bendiocarb. All assayed vector populations were fully susceptible to alpha-cypermethrin, pirimiphos-methyl, clothianidin and chlorfenapyr.  Plasmodium falciparum  infection was detected in 7.3% (37/508) of mosquitoes tested. The L1014F  kdr  mutation was found in 100% of a sub-sample of 60 mosquitoes, supporting its fixation in the region. The N1575Y mutation was identified in 20% (113/561) of individuals, with ongoing selection evidenced by significant deviations from Hardy–Weinberg equilibrium. The G119S  Ace - 1  mutation was detected in 62.1% (18/29) of mosquitoes tested and was highly predictive of bendiocarb bioassay survival. The metabolic resistance genes,  CYP6M2 ,  CYP6P3  and  GSTD3 , were found to be overexpressed in wild resistant and susceptible  An. gambiae  sensu stricto populations, compared to a susceptible G3 colony. Furthermore,  CYP6P3  was significantly overexpressed in bendiocarb survivors, implicating its potential role in carbamate resistance in Faranah.    Conclusions  Identification of intense resistance to permethrin and deltamethrin in Faranah, is of concern, as the Guinea National Malaria Control Programme (NMCP) relies exclusively on the distribution of pyrethroid-treated LLINs for vector control. Study findings will be used to guide current and future control strategies in the region.

Characterizing the molecular and metabolic mechanisms of insecticide resistance in Anopheles gambiae in Faranah, Guinea