The Role of Detoxification Enzymes in the Adaptation of the Major Malaria Vector Anopheles gambiae (Giles; Diptera: Culicidae) to Polluted Water.

The main malaria vectors in sub-Saharan Africa, the Anopheles gambiae (Giles; Diptera: Culicidae), normally breed in clean water sources. However, evidence suggests an on-going adaptation of Anopheline species to polluted breeding habitats in urban settings. This study aimed at understanding the adaptation to breeding in water bodies with different qualities, in five selected mosquito breeding sites in urban Accra, Ghana. The study sites were also evaluated for the WHO water-quality parameters as a measure of pollution, and insecticide residues. Field mosquitoes were evaluated for five genes; CYP6P3, CYP4H19, CYP4H24, GSTD1-4, and ABCC11-associated with insecticide detoxification-using quantitative RT-PCR, as well as Mono-oxygenase, Alpha Esterase, Glutathione S-transferase, and insensitive acetylcholinesterase (AChE) using biochemical enzyme assays. The lab-reared, insecticide susceptible An. gambiae Kisumu strain was bred in the most polluted water source for 10 generations and evaluated for the same genes and enzymes. The results revealed that the fold expression of the genes was higher in the larvae compared with the adults. The results also suggest that detoxification enzymes could be involved in the adaptation of An. gambiae to polluted breeding sites. Correlation analysis revealed a highly positive significant correlation between calcium levels and all five genes (P < 0.05). Stepwise linear regression to understand which of the variables predicted the expression of the genes revealed that sulphate was responsible for ABCC11 and CYP4H24, alkalinity for GSTD1-4, and calcium for CYP4H19 and CYP6P3. The detailed genetic basis of this adaptation need to be further investigated. A further understanding of this adaptation may provide outlooks for controlling malaria and other disease vectors adapted to polluted breeding water sources.

Variations in the quality of malaria-specific antibodies with transmission intensity in a seasonal malaria transmission area of Northern Ghana.

INTRODUCTION: Plasmodium falciparum induced antibodies are key components of anti-malarial immunity in malaria endemic areas, but their antigen targets can be polymorphic. Induction of a high proportion of strain-specific antibodies will limit the recognition of a broad diversity of parasite strains by these responses. There are indications that circulating parasite diversity varies with malaria transmission intensity, and this may affect the specificity of elicited anti-malarial antibodies. This study therefore assessed the effect of varying malaria transmission patterns on the specificity of elicited antibody responses and to identify possible antibody correlates of naturally acquired immunity to malaria in children in an area of Ghana with seasonal malaria transmission. METHODS: This retrospective study utilized plasma samples collected longitudinally at six time points from children aged one to five years. Multiplex assays were used to measure antibody levels against four P. falciparum AMA 1 variants (from the 3D7, FVO, HB3 and CAMP parasite strains) and the 3D7 variant of the EBA 175 region II antigen and the levels compared between symptomatic and asymptomatic children. The relative proportions of cross-reactive and strain-specific antibodies against the four AMA 1 variants per sampling time point were assessed by Bland-Altman plots. The levels of antibodies against allelic AMA1 variants, measured by singleplex and multiplex luminex assays, were also compared. RESULTS: The data show that increased transmission intensity is associated with higher levels of cross-reactive antibody responses, most likely a result of a greater proportion of multiple parasite clone infections during the high transmission period. Anti-AMA1 antibodies were however associated with a history of infection rather than protection in this age group. CONCLUSION: The data contribute to understanding the underlying mechanism of the acquisition of strain-transcending antibody immunity following repeated exposure to diverse parasite strains.