ArticleJournal of virology2020
A Polyuridine Insertion in the 3' Untranslated Region of Classical Swine Fever Virus Activates Immunity and Reduces Viral Virulence in Piglets.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Gestational timing and vaccine platform shape maternally derived neutralizing immunity and vaccine RNA detection in piglets following maternal vaccination with C-strain or FlagT4G against classical swine fever.Frontiers in veterinary science · 2026Article
- PorvacVaccines · 2025Article
- Gene Expression Signatures of Porcine Bone Marrow-Derived Antigen-Presenting Cells Infected with Classical Swine Fever Virus.Viruses · 2025Article
- Sublingual immunization with E2-CD154 protein and the STING agonist c-di-AMP confers protection against classical swine fever virus in pigs.Frontiers in cellular and infection microbiology · 2025Article
- Evolutionary-Related High- and Low-Virulent Classical Swine Fever Virus Isolates Reveal Viral Determinants of Virulence.Viruses · 2024Article
- Pathogenicity of a novel classical swine fever LOM vaccine-derived virus isolated on Jeju Island, South Korea.Veterinary medicine and science · 2022Article
- The FlagT4G Vaccine Confers a Strong and Regulated Immunity and Early Virological Protection against Classical Swine Fever.Viruses · 2022Article
- Removal of the EJournal of virology · 2022Article
- Abrogation of the RNase activity of EVirulence · 2021Article
- TNF-Mediated Inhibition of Classical Swine Fever Virus Replication Is IRF1-, NF-κB- and JAK/STAT Signaling-Dependent.Viruses · 2021Article
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- Foetal Immune Response Activation and High Replication Rate during Generation of Classical Swine Fever Congenital Infection.Pathogens (Basel, Switzerland) · 2020Article
- High-Resolution Profiling of Innate Immune Responses by Porcine Dendritic Cell SubsetsFrontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low-virulence classical swine fever virus (CSFV) strains make CSF eradication particularly difficult. Few data are available on the molecular determinants of CSFV virulence. The aim of the present study was to assess a possible role for CSFV virulence of a unique, uninterrupted 36-uridine (poly-U) sequence found in the 3' untranslated region (3' UTR) of the low-virulence CSFV isolate Pinar de Rio (PdR). To this end, a pair of cDNA-derived viruses based on the PdR backbone were generated, one carrying the long poly-U insertion in the 3' UTR (vPdR-36U) and the other harboring the standard 5 uridines at this position (vPdR-5U). Two groups of 20 5-day-old piglets were infected with vPdR-36U and vPdR-5U. Ten contact piglets were added to each group. Disease progression, virus replication, and immune responses were monitored for 5 weeks. The vPdR-5U virus was significantly more virulent than the vPdR-36U virus, with more severe disease, higher mortality, and significantly higher viral loads in serum and body secretions, despite similar replication characteristics in cell culture. The two viruses were transmitted to all contact piglets. Ninety percent of the piglets infected with vPdR-36U seroconverted, while only one vPdR-5U-infected piglet developed antibodies. The vPdR-5U-infected piglets showed only transient alpha interferon (IFN-α) responses in serum after 1 week of infection, while the vPdR-36U-infected piglets showed sustained IFN-α levels during the first 2 weeks. Taken together, these data show that the 3' UTR poly-U insertion acquired by the PdR isolate reduces viral virulence and activates the innate and humoral immune responses without affecting viral transmission.
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