ArticleFrontiers in immunology2022
2B and 3C Proteins of Senecavirus A Antagonize the Antiviral Activity of DDX21
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Determinants of Senecavirus A Pathogenesis: From Viral Genome to ANTXR1, Immunity, and Programmed Cell Death.Viruses · 2026Review
- Virulence determinant of Senecavirus A: 3C protein functions as a protease to cleave viral polyprotein and host factors.Virulence · 2025Review
- 3A and 2B proteins of SVA play chess game with host restriction factor DDX23 by apoptotic pathway.Journal of virology · 2025Article
- DEAD-box RNA helicase 10 inhibits porcine circovirus type 3 replication by interacting with the viral capsid protein and activating interferon responses.Journal of virology · 2025Article
- The liver-specific long noncoding RNA FAM99B inhibits ribosome biogenesis and cancer progression through cleavage of dead-box Helicase 21.Cell death & disease · 2025Article
- The DEAD-box RNA helicase 27 negatively regulates the replication of porcine reproductive and respiratory syndrome virus by mediating GP2a autophagy degradation and inducing interferon-β production.Frontiers in immunology · 2025Article
- Using reverse genetics tool for study of Senecavirus A: pros and cons.Frontiers in veterinary science · 2025Article
- DDX21 at the Nexus of RNA Metabolism, Cancer Oncogenesis, and Host-Virus Crosstalk: Decoding Its Biomarker Potential and Therapeutic Implications.International journal of molecular sciences · 2024Review
- Comparative transcriptomics analysis on Senecavirus A-infected and non-infected cells.Frontiers in veterinary science · 2024Article
- DEAD-box RNA helicase 21 interacts with porcine circovirus type 2 Cap protein and facilitates viral replication.Frontiers in microbiology · 2024Article
- Seneca Valley virus 3CFrontiers in microbiology · 2023Review
- The game between host antiviral innate immunity and immune evasion strategies of senecavirus A - A cell biological perspective.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senecavirus A (SVA), also known as Seneca Valley virus, is a recently discovered picornavirus that can cause swine vesicular disease, posing a great threat to the global swine industry. It can replicate efficiently in cells, but the molecular mechanism remains poorly understood. This study determined the host's differentially expressed proteins (DEPs) during SVA infection using dimethyl labeling based on quantitative proteomics. Among the DE proteins, DDX21, a member of the DEAD (Asp-Glu-Ala-Asp)-box RNA helicase (DDX) family, was downregulated and demonstrated inhibiting SVA replication by overexpression and knockdown experiment. To antagonize this antiviral effect of DDX21, SVA infection induces the degradation of DDX21 by 2B and 3C proteins. The Co-IP results showed that 2B and 3C did not interact with DDX21, suggesting that the degradation of DDX21 did not depend on their interaction. Moreover, the 3C protein protease activity was necessary for the degradation of DDX21. Furthermore, our study revealed that the degradation of DDX21 by 2B and 3C proteins of SVA was achieved through the caspase pathway. These findings suggest that DDX21 was an effective antiviral factor for suppressing SVA infection and that SVA antagonized its antiviral effect by degrading DDX21, which will be useful to guide further studies into the mechanism of mutual regulation between SVA and the host.
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