ArticleFrontiers in immunology2022
H7N9 bearing a mutation in the nucleoprotein leads to increased pathology in chickens.
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 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, 4 citations in OpenAlex.
- Genetic insights into avian influenza resistance in Jeju Island chickens: the roles of Mx1 and oligoadenylate synthetase-like single nucleotide polymorphisms.Journal of animal science and technology · 2025Article
- Knowledge, attitudes, and practices regarding avian influenza among poultry farmers near migratory bird habitats in Guidong County, China.Frontiers in public health · 2025Article
- Article
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Authors and funding
18 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The zoonotic H7N9 avian influenza (AI) virus first emerged in 2013 as a low pathogenic (LPAI) strain, and has repeatedly caused human infection resulting in severe respiratory illness and a mortality of ~39% (>600 deaths) across five epidemic waves. This virus has circulated in poultry with little to no discernible clinical signs, making detection and control difficult. Contrary to published data, our group has observed a subset of specific pathogen free chickens infected with the H7N9 virus succumb to disease, showing clinical signs consistent with highly pathogenic AI (HPAI). Viral genome sequencing revealed two key mutations had occurred following infection in the haemagglutinin (HA 226 L>Q) and nucleoprotein (NP 373 A>T) proteins. We further investigated the impact of the NP mutation and demonstrated that only chickens bearing a single nucleotide polymorphism (SNP) in their IFITM1 gene were susceptible to the H7N9 virus. Susceptible chickens demonstrated a distinct loss of CD8
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