Environmental Engineering Reference
In-Depth Information
Every year, 50-100 million dengue infections world-wide causing from 20,000 to
25,000 deaths from dengue and hemorrhagic fever are recorded [1]. As there is still
no medicine and effi cient vaccine available, vector control by the recourse of envi-
ronmental management, educational programs, and the use of chemical and biologi-
cal agents, remains the only method to reduce the risk of dengue virus transmission
[1]. Unfortunately, most of dengue vector control programs implemented worldwide
are facing operational challenges with the emergence and development of insecticide
resistance in
Ae. aegypti
[2] and
Ae. albopictus
[3]. Resistance of
Ae. aegypti
to in-
secticides has been reported in many regions including Southeast Asia [4, 5], Latin
America, [6] and the Caribbean [7].
Inherited resistance to chemical insecticides in mosquitoes is mainly the conse-
quence of two distinct mechanisms: the alteration of target sites inducing insensitivity
to the insecticide (target-site resistance) and/or an increased metabolism of the insec-
ticide (metabolic-based resistance) [8]. Metabolic-based resistance involves the bio-
transformation of the insecticide molecule by enzymes and is now considered as a key
resistance mechanism of insects to chemical insecticides [8, 9]. This mechanism may
result from two distinct but additive genetic events: (i) a mutation of the enzyme pro-
tein sequence leading to a better metabolism of the insecticide, and/or (ii) a mutation
in a non-coding regulatory region leading to the over-production of an enzyme capable
of metabolizing the insecticide. So far, only the second mechanism has been clearly
associated with the resistant phenotype in mosquitoes. Three large enzyme families,
the cytochrome P450 monooxygenases (P450s), glutathione S-transferases (GSTs) and
carboxy/cholinesterases (CCEs) have been implicated in the metabolism of insecticides
[8, 10-12]. The rapid expansion and diversifi cation of these so-called “detoxifi cation
enzymes” in insects is likely to be the consequence of their adaptation to a broad range
of natural xenobiotics found in their environment such as plant toxins [13]. These en-
zymes have also been involved in mosquito response to various anthropogenic xenobi-
otics such as heavy metals, organic pollutants, and chemical insecticides [14-16].
Although identifying metabolic resistance is possible by toxicological and bio-
chemical techniques, the large panel of enzymes potentially involved together with
their important genetic and functional diversity makes the understanding of the molec-
ular mechanisms and the role of particular genes a challenging task. As more mosquito
genomes have been sequenced and annotated [17, 18], the genetic diversity of genes
encoding mosquito detoxifi cation enzymes has been unraveled and new molecular
tools such as the
Aedes
and
Anopheles
“detox chip” microarrays allowing the analysis
of the expression pattern of all detoxifi cation genes simultaneously have been devel-
oped [19, 20]. These specifi c microarrays were successfully used to identify detoxi-
fi cation genes putatively involved in metabolic resistance in various laboratory and
fi eld-collected mosquito populations resistant to insecticides [19-24].
In Latin America and the Caribbean, several
Ae. aegypti
populations show strong
resistance to pyrethroid, carbamate, and organophosphate insecticides correlated with
elevated activities of at least one detoxifi cation enzyme family [25-28]. In addition,
several points of non-synonymous mutations in the gene encoding the trans-membrane
voltage-gated sodium channel (
kdr
mutations) have been described and showed to
confer resistance to pyrethroids and DDT [27, 29].
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