ArticleFrontiers in microbiology2018
C57BL/6J and C57BL/6NJ Mice Are Differentially Susceptible to Inflammation-Associated Disease Caused by Influenza A Virus.
Article in Frontiers in microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 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
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- Type I interferon production in myeloid cells is regulated by factors independent of Ptpn22.ImmunoHorizons · 2025Article
- Brief introduction in phenotypic and genetic differences of C57BL/6 and BALB/c mice substrains.Animal models and experimental medicine · 2025Review
- Enhanced neurotropism of bovine H5N1 compared to the Vietnam H5N1 isolate in C57BL/6J mice.Npj viruses · 2025Article
- Multiplex Detection of SNPs for Genetic Monitoring in Laboratory Mice by Luminex xTAG Assay.Genes · 2024Article
- Comparative pathogenicity of influenza virus-induced pneumonia mouse model following intranasal and aerosolized intratracheal inoculation.Virology journal · 2024Article
- Need for standardization of Influenza A virus-induced cell death in vivo to improve consistency of inter-laboratory research findings.Cell death discovery · 2024Review
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- Severe respiratory viral infections: T-cell functions diverging from immunity to inflammation.Trends in microbiology · 2023Review
- MLKL deficiency protects against low-grade, sterile inflammation in aged mice.Cell death and differentiation · 2023Article
- C57Bl/6N mice have an attenuated lung inflammatory response to dsRNA compared to C57Bl/6J and BALB/c mice.Journal of inflammation (London, England) · 2023Article
- FcRn-Targeted Mucosal Vaccination against Influenza Virus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Substrains matter in phenotyping of C57BL/6 mice.Experimental animals · 2021Review
- Human Properdin Released By Infiltrating Neutrophils Can Modulate Influenza A Virus Infection.Frontiers in immunology · 2021Article
- Distinct Phenotypes Induced by Different Degrees of Transverse Aortic Constriction in C57BL/6N Mice.Frontiers in cardiovascular medicine · 2021Article
- Dabigatran activates inflammation resolution by promoting fibrinogen-like protein 2 shedding and RvD5Theranostics · 2021Article
- Affective Disruption During Forced Ethanol Abstinence in C57BL/6J and C57BL/6NJ Mice.Alcoholism, clinical and experimental research · 2020Article
- Dendritic cell NLRC4 regulates influenza A virus-specific CD4 T cell responses through FasL expression.The Journal of clinical investigation · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Influenza viruses cause seasonal epidemics and sporadic pandemics, and are a major burden on human health. To develop better countermeasures and improve influenza disease outcomes, a clearer understanding of influenza pathogenesis is necessary. Host genetic factors have emerged as potential regulators of human influenza disease susceptibility, and in the mouse model, genetic background has been clearly linked to influenza pathogenicity. Here, we show that C57BL/6J mice are significantly more susceptible to disease caused by a 2009 pandemic H1N1 virus, an H7N9 virus, and a highly pathogenic H5N1 influenza virus compared to the closely related substrain, C57BL/6NJ. Mechanistically, influenza virus infection in C57BL/6J mice results in earlier presentation of edema, increased immune cell infiltration, higher levels of inflammatory cytokines, greater tissue damage, and delayed activation of regenerative processes in infected lung tissues compared to C57BL/6NJ mice. These differences are not dependent on virus replication levels. Six genes with known coding region differences between C57BL/6J and C57BL/6NJ strains exhibit increased transcript levels in influenza virus-infected mouse lungs, suggesting potential contributions to regulation of disease susceptibility. This work uncovers a previously unappreciated difference in disease susceptibility between the closely related C57BL/6J and C57BL/6NJ mice, which may be exploited in future studies to identify host factors and/or specific genetic elements that regulate host-dependent inflammatory mechanisms involved in influenza virus pathogenicity.
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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.