ArticleJournal of virology2025
DEAD-box RNA helicase 10 inhibits porcine circovirus type 3 replication by interacting with the viral capsid protein and activating interferon responses.
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 2 papers.
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
2 citing papers in PubMed.
- DDX10 RNA Helicase: Structure, Function, and Oncogenic Roles Across Solid and Hematologic Tumors.Genes · 2026Review
- 3A and 2B proteins of SVA play chess game with host restriction factor DDX23 by apoptotic pathway.Journal of virology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Porcine circovirus type 3 (PCV3) is an emerging pathogen that causes porcine dermatitis and nephropathy syndrome-like symptoms, multisystemic inflammation, and reproductive failure. The PCV3 capsid (Cap) protein interacts with DEAD-box RNA helicase 10 (DDX10), a protein that functions primarily through regulating interferon (IFN)-β production to exert its antiviral activity. However, how the interaction between DDX10 and PCV3 Cap regulates viral replication remains unknown. We used Western blotting, interaction assays, and knockdown analyses to observe impaired PCV3 proliferation in transiently DDX10-overexpressing cells, as indicated by decreased viral protein expression levels and virus production. In contrast, PCV3 replication increased upon small interfering RNA-mediated
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Registered trials
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