title: Immune transcript variations among Aedes aegypti populations with distinct susceptibility to dengue virus serotype 2.
abstract: The innate immune response of insects is one of the factors that may dictate their susceptibility to viral infection. Two immune signaling pathways, Toll and JAK-STAT, and the RNA interference (RNAi) pathway are involved in Aedes aegypti responses against dengue virus (DENV), however natural differences in these antiviral defenses among mosquito populations have not been studied. Here, two field Ae. aegypti populations from distinct ecological environments, one from Recife and the other from Petrolina (Brazil), and a laboratory strain were studied for their ability to replicate a primary isolate of dengue virus serotype 2 (DENV-2). Virus infectivity and replication were determined in insect tissues collected after viral exposure through reverse-transcription real time PCR (RT-PCR). The expression of a transcript representing these defense mechanisms (Toll, JAK-STAT and RNAi) in the midgut and fat body was studied with RT-PCR to evaluate variations in innate immune mechanisms possibly employed against DENV. Analyses of infection rates indicated that the field populations were more susceptible to DENV-2 infection than the lab strain. There were distinct expression patterns among mosquito populations, in both control and infected insects. Moreover, lower expression of immune molecules in DENV-2-infected insects compared to controls was observed in the two field populations. These results suggest that natural variations in vector competence against DENV may be partly due to differences in mosquito defense mechanisms, and that the down-regulation of immune transcripts after viral infection depends on the insect strain.
authors.affiliation: Departamento de Entomologia, Centro de Pesquisas Aggeu Magalhães, Fundação Oswaldo Cruz (Fiocruz-Pernambuco), Recife, Brazil. danilo@cpqam.fiocruz.br
authors.forename: D
authors.initials: D
authors.lastname: Carvalho-Leandro
authors.forename: C F J
authors.initials: CF
authors.lastname: Ayres
authors.forename: D R D
authors.initials: DR
authors.lastname: Guedes
authors.forename: L
authors.initials: L
authors.lastname: Suesdek
authors.forename: M A V
authors.initials: MA
authors.lastname: Melo-Santos
authors.forename: C F
authors.initials: CF
authors.lastname: Oliveira
authors.forename: M T
authors.initials: MT
authors.lastname: Cordeiro
authors.forename: L N
authors.initials: LN
authors.lastname: Regis
authors.forename: E T
authors.initials: ET
authors.lastname: Marques
authors.forename: L H
authors.initials: LH
authors.lastname: Gil
authors.forename: T
authors.initials: T
authors.lastname: Magalhaes
mesh_terms: D000330:Aedes / Q000276:immunology* / Q000821:virology*; D000818:Animals; D001938:Brazil; D003716:Dengue Virus / Q000276:immunology*; D005216:Fat Body / Q000276:immunology / Q000821:virology; D041981:Gastrointestinal Tract / Q000276:immunology / Q000821:virology; D020869:Gene Expression Profiling; D054884:Host-Pathogen Interactions; D007113:Immunity, Innate; D060888:Real-Time Polymerase Chain Reaction