Table 1.
Population | Genotypes | Target-site allele frequency, %* | |||||
No. of specimens | Molecular form, % | No. of specimens | 1014F/F | 1014F/L | 10114L/L | ||
M/M | S/S | ||||||
Malabo 2004† | — | 36 | 64 | 4,500 | 14 | 41 | 45 |
Malabo 2011 | 75 | 100 | 0 | 75 | 28.5 | 57.14 | 14.3 |
Malabo hospital 2015 | 16 | 100 | 0 | 16 | 100 | 0 | 0 |
Malabo industrial 2015 | 16 | 100 | 0 | 16 | 100 | 0 | 0 |
M, An. coluzzii (M form); S, An. gambiae s.s. (S form).
Data from Hemingway et al., 2013 (23).
Mutations L1014S and N1575Y on the voltage-gated sodium channel, as well as mutation G119S on acetylcholinesterase, were absent in all alleles (n > 200) genotyped in both 2011 and 2015. F/F, individuals homozygous for mutation L1014F on the voltage-gated sodium channel; F/L, heterozygotes; L/L, homozygous individuals for the WT (i.e., susceptible) allele.