Liu Y, Xu J, Wei C, Xu Y, Lyu C, Sun M, Zheng Y, C. Detection of H1N1 Influenza Virus in the Bile of a Severe Influenza Mouse Model. Influenza Other Respir Viruses. 2024 Oct;18(10):e7
Aims: Influenza virus infection may lead to fatal complications including multi-organ failure and sepsis. The influenza virus was detected in various extra-pulmonary organs in autopsy studies during the 2009 pandemic. However, limited research has been conducted on the presence of viral particle or viral components in the peripheral blood.
Methods and results: We established a mouse model for severe H1N1 influenza. The bile and blood samples were collected over time and inoculated into embryonated chicken eggs. We detected live influenza virus in bile and blood samples in early infection. Immunofluorescence showed influenza viral components in the liver tissue. No live virus was isolated in the bile in mice intragastrically administered with influenza virus, indicating that the virus was spread from the blood stream. Targeted metabolomics analysis of bile acid and liver tissues showed that a secondary bile acid (3-dehydrocholic acid) was decreased after influenza H1N1 infection. Genes related with fatty acid metabolism and bile secretion pathways were down-regulated in liver after influenza virus infection.
Conclusion: Our study indicated that influenza virus viremia is present in severe influenza, and that the liver is a target organ for influenza viral sepsis.
Methods and results: We established a mouse model for severe H1N1 influenza. The bile and blood samples were collected over time and inoculated into embryonated chicken eggs. We detected live influenza virus in bile and blood samples in early infection. Immunofluorescence showed influenza viral components in the liver tissue. No live virus was isolated in the bile in mice intragastrically administered with influenza virus, indicating that the virus was spread from the blood stream. Targeted metabolomics analysis of bile acid and liver tissues showed that a secondary bile acid (3-dehydrocholic acid) was decreased after influenza H1N1 infection. Genes related with fatty acid metabolism and bile secretion pathways were down-regulated in liver after influenza virus infection.
Conclusion: Our study indicated that influenza virus viremia is present in severe influenza, and that the liver is a target organ for influenza viral sepsis.
See Also:
Latest articles in those days:
- Comprehensive Molecular Epidemiology of Influenza Viruses in Brazil: Insights from a Nationwide Analysis 1 days ago
- Pandemic preparedness of effective vaccines for the outbreak of newly H5N1 highly pathogenic avian influenza virus 1 days ago
- The PB1 protein of H9N2 influenza A virus inhibits antiviral innate immunity by targeting MAVS for TRIM25-mediated autophagic degradation 1 days ago
- The evolution of hemagglutinin-158 and neuraminidase-88 glycosylation sites modulates antigenicity and pathogenicity of clade 2.3.2.1 H5N1 avian influenza viruses 1 days ago
- Evidence of Influenza A(H5N1) Spillover Infections in Horses, Mongolia 1 days ago
[Go Top] [Close Window]