ArticleVirus research2014
The origin of the PB1 segment of swine influenza A virus subtype H1N2 determines viral pathogenicity in mice.
Article in Virus research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Genetic and biological characterization of H9N2 avian influenza viruses isolated from swine in China.BMC veterinary research · 2026Article
- Coinfection and nonrandom recombination drive the evolution of swine enteric coronaviruses.Emerging microbes & infections · 2024Article
- Swine influenza A virus isolates containing the pandemic H1N1 origin matrix gene elicit greater disease in the murine model.Microbiology spectrum · 2024Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Swine appear to be a key species in the generation of novel human influenza pandemics. Previous pandemic viruses are postulated to have evolved in swine by reassortment of avian, human, and swine influenza viruses. The human pandemic influenza viruses that emerged in 1957 and 1968 as well as swine viruses circulating since 1998 encode PB1 segments derived from avian influenza viruses. Here we investigate the possible role in viral replication and virulence of the PB1 gene segments present in two swine H1N2 influenza A viruses, A/swine/Sweden/1021/2009(H1N2) (sw 1021) and A/swine/Sweden/9706/2010(H1N2) (sw 9706), where the sw 1021 virus has shown to be more pathogenic in mice. By using reverse genetics, we swapped the PB1 genes of these two viruses. Similar to the sw 9706 virus, chimeric sw 1021 virus carrying the sw 9706 PB1 gene was not virulent in mice. In contrast, replacement of the PB1 gene of the sw 9706 virus by that from sw 1021 virus resulted in increased pathogenicity. Our study demonstrated that differences in virulence of swine influenza virus subtype H1N2 are attributed at least in part to the PB1 segment.
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Registered trials
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