Related Experiment Videos
Mouse hepatitis virus type 3 infection provokes a decrease in the number of sinusoidal endothelial cell fenestrae
A M Steffan1, C A Pereira, A Bingen
1Unité INSERM 74 et Institut de Virologie de la Faculté de Médecine, Strasbourg, France.
Hepatology (Baltimore, Md.)
|August 1, 1995
Summary
Mouse hepatitis virus 3 (MHV3) infection significantly reduces liver endothelial cell fenestrae, impairing liver function. This viral-induced fenestration loss impacts liver sieve barrier function.
Area of Science:
- Hepatology
- Virology
- Cell Biology
Background:
- Hepatic endothelial cell fenestrations are crucial for liver function, acting as a sieve for blood-parenchyma exchange.
- Pathological events can alter fenestrations, leading to liver dysfunction.
Purpose of the Study:
- To investigate the effect of mouse hepatitis virus 3 (MHV3) infection on hepatic endothelial cell fenestrae.
- To determine if MHV3 infection alters liver sieve barrier function.
Main Methods:
- Infection of sinusoidal endothelial cells with MHV3 in vivo and in vitro.
- Scanning electron microscopy and cryofracture to visualize fenestrae.
- Assessment of fenestration changes in susceptible and resistant mouse models.
Main Results:
- MHV3 infection caused a significant decrease in hepatic endothelial cell fenestrae.
- The loss of fenestrae was observed both in vivo and in vitro.
- Cytochalasin B did not reverse the fenestral changes.
- Fenestration loss correlated with productive viral replication, not observed in resistant mice or after immunization with a non-replicating mutant.
Conclusions:
- Productive MHV3 infection of liver endothelial cells leads to extensive loss of fenestrations.
- This viral-induced alteration of fenestrae likely causes significant liver functional perturbations.