ArticleVirulence2018
Altered virulence of Highly Pathogenic Avian Influenza (HPAI) H5N8 reassortant viruses in mammalian models.
Article in Virulence, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Rule-based meta-analysis reveals the major role of PB2 in influencing influenza A virus virulence in mice.BMC genomics · 2019Pooled it
- Article
- Age-dependent pathogenic characteristics of SARS-CoV-2 infection in ferrets.Nature communications · 2022Article
- Age-dependent pathogenic characteristics of SARS-CoV-2 infection in ferrets.Research square · 2021Article
- Infection and Rapid Transmission of SARS-CoV-2 in Ferrets.Cell host & microbe · 2020Article
- Human surveillance and phylogeny of highly pathogenic avian influenza A(H5N8) during an outbreak in poultry in South Africa, 2017.Influenza and other respiratory viruses · 2020Article
- Avian influenza overview November 2017 - February 2018.EFSA journal. European Food Safety Authority · 2018Article
- Article
- Avian influenza overview September - November 2017.EFSA journal. European Food Safety Authority · 2017Article
- An overview of preclinical animal models for SARS-CoV-2 pathogenicity.The Indian journal of medical researchReview
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently identified highly pathogenic avian influenza (HPAI) H5N8 viruses (clade 2.3.4.4) are relatively low to moderately pathogenic in mammalian hosts compared with HPAI H5N1 viruses. In this study, we generated reassortant viruses comprised of A/MD/Korea/W452/2014(H5N8) with substitution of individual genes from A/EM/Korea/W149/2006(H5N1) to understand the contribution of each viral gene to virulence in mammals. Substituting the PB2 gene segment or the NA gene segment of the H5N8 virus by that from the H5N1 virus resulted in significantly enhanced pathogenicity compared with the parental H5N8 virus in mice. Of note, substitution of the PB2 gene segment of the H5N8 virus by that from the H5N1 virus resulted in a 1000-fold increase in virulence for mice compared with the parental virus (MLD
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