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Pathology of influenza hepatitis in susceptible and genetically resistant mice
Abstract:
Mice resistant (homozygous or heterozygous for the gene Mx) and mice susceptible to the lethal effect of influenza viruses were inoculated intraperitoneally and intraportally with a hepatotropic variant of influenza A virus. Disease evolution was followed histologically and by immunofluorescence. In susceptible animals, rapidly spreading foci of hepatocyte necrosis with little inflammatory infiltration was observed. Death occurred on the 3rd day, when the entire liver was involved. In resistant animals foci became detectable later, and were fewer and smaller. They were infiltrated by cells morphologically resembling liver macrophages (Kupffer cells), and they regressed from the 4th day after infection. Barriers to virus spread appeared to be present at all stages of the disease.
Insights
Mice resistant to influenza virus showed fewer liver lesions and survived longer than susceptible mice. Resistance involves early detection and infiltration of liver macrophages, preventing virus spread.
Area of Science:
- Virology
- Immunology
- Hepatology
Background:
- Influenza A virus can cause severe liver disease.
- Genetic factors influence host susceptibility to viral infections.
- The Mx gene confers resistance to certain viruses.
Purpose of the Study:
- To investigate the role of host resistance in influenza A virus-induced liver disease.
- To compare disease progression in susceptible and resistant mice.
- To elucidate the mechanisms of viral resistance in the liver.
Main Methods:
- Inoculation of hepatotropic influenza A virus in resistant and susceptible mice.
- Histological examination of liver tissues.
- Immunofluorescence staining for viral detection and cellular infiltration.
Main Results:
- Susceptible mice exhibited rapid hepatocyte necrosis and widespread liver involvement, leading to death by day 3.
- Resistant mice displayed delayed, smaller foci of necrosis with Kupffer cell infiltration and lesion regression by day 4.
- Evidence suggests intrinsic barriers to viral spread in resistant hosts.
Conclusions:
- Host genetic resistance, mediated by the Mx gene, significantly impacts influenza A virus liver pathogenesis.
- Kupffer cells play a crucial role in limiting viral spread and promoting recovery in resistant mice.
- Understanding these resistance mechanisms could inform therapeutic strategies against severe influenza.