Abstract
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. 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 with plaque assay test and
negative stain with electronic microscopy 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. Our study
indicated that influenza virus viremia is present in severe influenza,
and that the liver is a target organ for influenza viral sepsis.