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Mouse hepatitis virus type 3 infection provokes a decrease in the number of sinusoidal endothelial cell fenestrae both in vivo and in vitro
Author(s) -
Steffan AnneMarie,
Pereira Carlos Augusto,
Bingen Annick,
Valle Michele,
Martin JeanPierre,
Koehren Françoise,
Royer Cathy,
Gendrault JeanLouis,
Kirn André
Publication year - 1995
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840220204
Subject(s) - in vivo , mouse hepatitis virus , biology , in vitro , endothelial stem cell , virus , endothelium , parenchyma , virology , microbiology and biotechnology , immunology , pathology , medicine , biochemistry , endocrinology , botany , disease , covid-19 , infectious disease (medical specialty)
Fenestrations of hepatic endothelial cells play an active role as a sieving barrier allowing extensive exchange between the blood and liver parenchyma. Alteraction of these structures may be induced in the course of various pathological events and provoke important perturbations of liver function. We demonstrate here that sinusoidal endothelial cells are permissive for mouse hepatitis virus 3 (MHV3) in vivo and in vitro and that this infection leads to a striking decrease in the number of fenestrae. The disappearance of these structures observed under scanning electron microscopy or in cryofracture preparations in vivo and in vitro cannot be reversed by the action of cytochalasin B on the microfilament network. The decrease in the porosity seems to be related directly to the productive infection of the endothelial cells, because it was not observed in A/J mice resistant to the virus and in susceptible BALB/c mice immunized with a thermosensitive mutant in which no viral replication occurs. In conclusion, a viral infection of liver endothelial cells may cause extensive loss of the fenestrations and thus lead to important functional pertubations. (Hepatology 1995; 22:395–401.)