ArticleJournal of virology2025
DENV-2 3'UTR dumbbell structure is a critical factor for viral infection and dissemination in
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Identification of Ligand-Responsive RNA G-Quadruplexes in the 3' UTRs of Dengue Virus Serotypes.Biomolecules · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Dengue virus (DENV) is a mosquito-borne flavivirus with the capability of replicating and spreading between vertebrate and invertebrate hosts, which poses a huge threat to global public health. Understanding the molecular mechanism of its replication and transmission in mosquitoes is crucial for controlling the dengue epidemic. The 3' untranslated region (UTR) has been identified as a mediator for viral replication, pathogenicity, and transmission, but its effect on DENV in the mosquito host remains unknown. This study investigated the role of the dumbbell (DB) structure within the 3'UTR of DENV-2 during mosquito infection. The results showed that the absence of the DB structure reduced DENV-2 viral replication efficiency in both mosquito cell lines and IMPORTANCE: Dengue virus (DENV) transmitted by Aedes mosquitoes threatens global health. This study focuses on the dumbbell (DB) structure in DENV-2's 3' untranslated region, which is crucial for viral replication and transmission in mosquitoes. We discovered that the absence of the DB structure reduces DENV-2's replication efficiency and impairs its ability to evade the mosquito midgut barrier. Transcriptome data suggest that the DB structure may facilitate viral escape by modulating the expression of Defensin A and Defensin C. Functional validation in C6/36 cells demonstrates that Defensin C acts as an inhibitor, suppressing the replication of DENV-2 with the absence of DB structure and revealing a novel RNA structure-mediated immune evasion strategy. The findings of this study highlight the critical role of the DB structure in DENV-2 adaptation to mosquito hosts and provide valuable insights into the mechanisms of flavivirus transmission and potential strategies for dengue control.
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