ArticleParasites & vectors2026
Dual functions of the Aedes aegypti ecdysone receptor in dengue virus replication and reproduction control.
Article in Parasites & vectors, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundThe ecdysone receptor (EcR) is a central regulator of mosquito physiology, best known for its role in vitellogenesis. However, its contribution to antiviral defense and dengue virus (DENV) replication in Aedes aegypti remains poorly understood.
methodsRNA interference was used to silence Aedes aegypti EcR (AaEcR). Effects on DENV replication, immune gene expression, ovarian development, vitellogenin (Vg) synthesis, and target of rapamycin (TOR) pathway activity were assessed using molecular, cellular, and phenotypic analyses.
resultsSilencing AaEcR markedly suppressed DENV replication, viral protein expression, and virion production. These antiviral effects coincided with increased expression of antimicrobial peptides and activation of innate immune pathways, indicating that AaEcR facilitates viral replication by dampening host defenses. In addition, AaEcR proved essential for reproductive output. Knockdown impaired ovarian development, reduced follicle size and number, and lowered egg production by ~30%, although egg viability was unaffected. At the molecular level, AaEcR depletion strongly reduced Vg transcription and protein abundance, along with decreased phosphorylation of S6 kinase, suggesting that AaEcR promotes fecundity through both transcriptional activation and TOR-Vg signaling.
conclusionsAaEcR functions as a dual regulator of mosquito biology, suppressing antiviral immunity while enhancing reproductive output. This tradeoff between immunity and fecundity highlights AaEcR as a promising molecular target for vector control. Disrupting EcR signaling could simultaneously reduce mosquito population size and limit arboviral transmission, offering a potential strategy for integrated management of mosquito-borne diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.