ArticleVirology2012
Both influenza hemagglutinin and polymerase acidic genes are important for delayed pandemic 2009 H1N1 virus clearance in the ferret model.
Article in Virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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
5 citing papers in PubMed, 9 citations in OpenAlex.
- PA and PA-X: two key proteins from segment 3 of the influenza viruses.Frontiers in cellular and infection microbiology · 2025Review
- Two amino acid residues in the N-terminal region of the polymerase acidic protein determine the virulence of Eurasian avian-like H1N1 swine influenza viruses in mice.Journal of virology · 2024Article
- A North American H7N3 Influenza Virus Supports Reassortment with 2009 Pandemic H1N1 and Induces Disease in Mice without Prior Adaptation.Journal of virology · 2016Article
- Swine Influenza Virus PA and Neuraminidase Gene Reassortment into Human H1N1 Influenza Virus Is Associated with an Altered Pathogenic Phenotype Linked to Increased MIP-2 Expression.Journal of virology · 2015Article
- Emergence of HA mutants during influenza virus pneumonia.International journal of clinical and experimental pathology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
We previously showed that a pandemic virus, A/Tennessee/560/09(H1N1), had the potential to adapt to human bronchial epithelial cells by the acquisition of hemagglutinin (HA) K154Q and polymerase acidic (PA) protein L295P mutations that conferred a more virulent phenotype. To better elucidate the role of each mutations, we generated recombinant viruses carrying single mutations or both mutations concurrently. The replication of all mutant viruses was significantly higher than that of the wild-type A/Tennessee/560/09 virus in human cells. The HA K154Q mutation reduced the receptor binding affinity of A/Tennessee/560/09 virus to 6-Su-6'SLN and biantennary 6'SLN receptors. In ferrets, H1N1 virus with HA K154Q and PA L295P mutations exhibited significantly higher titers in the upper respiratory tract compared to all other viruses 6 days post-infection. Our results suggest that both single mutations HA K154Q and PA L295P are necessary for delayed virus clearance of A/Tennessee/560/09(H1N1) influenza virus in a ferret animal model.
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Registered trials
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.