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Vector competence and innate immune responses to dengue virus infection in selected laboratory and field‐collected Stegomyia aegypti (= Aedes aegypti )
Author(s) -
SERRATO I. M.,
CAICEDO P. A.,
OROBIO Y.,
LOWENBERGER C.,
OCAMPO C. B.
Publication year - 2017
Publication title -
medical and veterinary entomology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 82
eISSN - 1365-2915
pISSN - 0269-283X
DOI - 10.1111/mve.12237
Subject(s) - biology , aedes aegypti , dengue fever , dengue virus , virology , serotype , vector (molecular biology) , virus , innate immune system , gene , immune system , immunology , genetics , ecology , recombinant dna , larva
Control of dengue virus (DenV) transmission, primarily based on strategies to reduce populations of the principle vector Stegomya aegypti (= Aedes aegypti ) (Diptera: Culicidae), is difficult to sustain over time. Other potential strategies aim to manipulate characteristics such as vector competence ( VC ), the innate capacity of the vector to transmit the virus. Previous studies have identified genetic factors, including differential expression of apoptosis‐related genes, associated with the refractory and susceptible phenotypes in selected strains of S. aegypti from Cali, Colombia. The present study was designed to evaluate the variability of VC in selected strains against different DenV serotypes and to determine whether field‐collected mosquitoes respond similarly to selected laboratory strains in terms of enhanced or reduced expression of apoptosis‐related genes. Vector competence differed between strains, but did not differ in response to different DenV serotypes. Differences in VC were observed among mosquitoes collected from different localities in Cali. The overexpression of the pro‐apoptosis genes, caspase 16 and Aedronc , was conserved in field‐collected refractory mosquitoes and the selected laboratory refractory strain. The results suggest that the apoptosis response is conserved among all refractory mosquitoes to inhibit the development of all DenV serotypes.