ArticleJournal of virology2019
Persistent Infection and Transmission of Senecavirus A from Carrier Sows to Contact Piglets.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 57 citations in OpenAlex.
- Serological and molecular evaluation of Senecavirus A (SVA) in pigs from farrow-to-finish farms in Minas Gerais, Brazil.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026Article
- 3A and 2B proteins of SVA play chess game with host restriction factor DDX23 by apoptotic pathway.Journal of virology · 2025Article
- Phylogenetic Characterization and Seroprevalence ofAnimals : an open access journal from MDPI · 2025Article
- Senecavirus A Incidence in U.S. Breeding Herds: A Decade of Surveillance Data.Animals : an open access journal from MDPI · 2025Article
- Phylogeographic Characterizations of Recent (2015-2023) Senecavirus A Isolates from Canada.Viruses · 2025Article
- Isolation and Characterization of Seneca Valley Virus From Pig Transboundary Spread to the Mink Infection.Transboundary and emerging diseases · 2025Article
- Pathogenicity of the First Buffalo-origin Senecavirus A in Conventional Piglets and Buffaloes.Transboundary and emerging diseases · 2025Article
- TRIM5 inhibits the replication of Senecavirus A by promoting the RIG-I-mediated type I interferon antiviral response.Veterinary research · 2024Article
- Senecavirus cetus a novel picornavirus isolated from cetaceans represents a major host switching to the marine environment.Npj viruses · 2024Article
- ZBP1 inhibits the replication of Senecavirus A by enhancing NF-κB signaling pathway mediated antiviral response in porcine alveolar macrophage 3D4/21 cells.Cellular & molecular biology letters · 2024Article
- Silencing RNA-Mediated Knockdown of IFITM3 Enhances Senecavirus A Replication.Pathogens (Basel, Switzerland) · 2024Article
- Construction and characterization of a full-length infectious clone of an emerging senecavirus A strain.Archives of virology · 2024Article
- Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA.Viruses · 2023Review
- Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I.PLoS pathogens · 2023Article
- Innate sensing of picornavirus infection involves cGAS-STING-mediated antiviral responses triggered by mitochondrial DNA release.PLoS pathogens · 2023Article
- The Evolution and Global Spatiotemporal Dynamics of Senecavirus A.Microbiology spectrum · 2022Article
- Development of an indirect ELISA using a novel linear epitope at the C-terminal region of the VP2 protein to specifically detect antibodies against Senecavirus A.Virology journal · 2022Article
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- 2B and 3C Proteins of Senecavirus A Antagonize the Antiviral Activity of DDX21Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senecavirus A (SVA) is a picornavirus that causes acute vesicular disease (VD), that is clinically indistinguishable from foot-and-mouth disease (FMD), in pigs. Notably, SVA RNA has been detected in lymphoid tissues of infected animals several weeks following resolution of the clinical disease, suggesting that the virus may persist in select host tissues. Here, we investigated the occurrence of persistent SVA infection and the contribution of stressors (transportation, immunosuppression, or parturition) to acute disease and recrudescence from persistent SVA infection. Our results show that transportation stress leads to a slight increase in disease severity following infection. During persistence, transportation, immunosuppression, and parturition stressors did not lead to overt/recrudescent clinical disease, but intermittent viremia and virus shedding were detected up to day 60 postinfection (p.i.) in all treatment groups following stress stimulation. Notably, real-time PCR and
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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.