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Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Mechanisms of pathogenicity of influenza A (H5N1) viruses in mice
1Emory University, Atlanta, GA 30329, USA.
Abstract:
Avian-like H5N1 influenza viruses isolated from humans in 1997 were shown to have two distinct pathogenic phenotypes in BALB/c mice, after intranasal inoculation and without prior adaptation to this host. To further understand the mechanisms of H5N1 pathogenicity, we investigated the consequences of the mute of viral inoculation on morbidity and mortality, viral replication in pulmonary and systemic organs, and lymphocyte depletion. This study demonstrates the importance of extrapulmonary spread and replication, particularly in the brain, for the lethality of H5N1 viruses.
Insights
Avian H5N1 influenza viruses showed varied pathogenicity in mice. Extrapulmonary viral spread, especially to the brain, is crucial for H5N1 virus lethality.
Area of Science:
- Virology
- Pathology
- Immunology
Background:
- Avian-like H5N1 influenza viruses were isolated from humans in 1997.
- These viruses exhibited distinct pathogenic phenotypes in BALB/c mice without host adaptation.
Purpose of the Study:
- To investigate the mechanisms of H5N1 pathogenicity.
- To understand the impact of viral inoculation route on disease outcomes.
Main Methods:
- Intranasal inoculation of BALB/c mice with H5N1 viruses.
- Assessment of morbidity, mortality, viral replication in organs, and lymphocyte depletion.
Main Results:
- H5N1 viruses displayed differential pathogenicity.
- Significant viral replication was observed in extrapulmonary organs, including the brain.
- Lymphocyte depletion was a notable consequence.
Conclusions:
- Extrapulmonary viral spread and replication, particularly in the brain, are critical determinants of H5N1 lethality.
- Understanding these mechanisms is vital for managing H5N1 influenza.
- The route of inoculation influences H5N1 pathogenesis.
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