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The effect of mouse hepatitis virus infection on the microcirculation of the liver
Abstract:
Mouse hepatitis virus type 3 infection results in strain-dependent liver disease. The effects of mouse hepatitis virus type 3 on the microcirculation of the liver in both fully susceptible (Balb/cJ) and fully resistant (A/J) mice were studied. In Balb/cJ mice, 6 to 12 hr following infection, abnormalities in liver blood flow were observed which consisted of granular blood flow in both terminal hepatic and terminal portal venules. In addition, sinusoidal microthrombi were present predominantly in periportal areas. By 24 to 48 hr, liver cell edema and small focal lesions were prominent. At 48 hr, thrombi and hepatocellular necrosis were widespread, and blood was shunted from damaged areas into patent sinusoids. In sharp contrast to these abnormal findings, normal streamlined blood flow was present in the resistant A/J animals at all time points following infection. Since large amounts of virus were demonstrated by immunofluorescene in and by recovery and growth from livers of both resistant and susceptible strains, the presence of the virus per se cannot explain the abnormalities observed.
Insights
Mouse hepatitis virus type 3 causes liver disease in susceptible mice by disrupting liver microcirculation. Resistant mice show normal blood flow, indicating virus presence alone doesn't cause disease.
Area of Science:
- Virology
- Hepatology
- Immunology
Background:
- Mouse hepatitis virus type 3 (MHV-3) infection leads to varied liver disease outcomes.
- Strain-dependent susceptibility in mice influences disease severity and pathology.
Purpose of the Study:
- To investigate the impact of MHV-3 on liver microcirculation in susceptible (Balb/cJ) and resistant (A/J) mouse strains.
- To determine if virus presence alone explains observed liver abnormalities.
Main Methods:
- Comparative study of liver microcirculation in MHV-3 infected Balb/cJ and A/J mice.
- Assessment of blood flow, microthrombi formation, and hepatocellular changes at various time points post-infection.
- Viral detection using immunofluorescence and recovery assays.
Main Results:
- Susceptible Balb/cJ mice exhibited granular blood flow, sinusoidal microthrombi, edema, and hepatocellular necrosis.
- Resistant A/J mice maintained normal liver blood flow throughout the study.
- High viral loads were detected in both susceptible and resistant strains, irrespective of pathology.
Conclusions:
- MHV-3 infection induces significant liver microcirculatory disturbances and hepatocellular damage in a strain-dependent manner.
- The observed pathology is not solely attributable to the presence of the virus but involves host-specific responses.
- Liver microvascular integrity plays a critical role in determining disease outcome during MHV-3 infection.