title: Mouse hepatitis virus type 3 infection provokes a decrease in the number of sinusoidal endothelial cell fenestrae both in vivo and in vitro.
abstract: Fenestrations of hepatic endothelial cells play an active role as a sieving barrier allowing extensive exchange between the blood and liver parenchyma. Alteration 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.
authors.affiliation: Unité INSERM 74 et Institut de Virologie de la Faculté de Médecine, Strasbourg, France.
authors.forename: A M
authors.initials: AM
authors.lastname: Steffan
authors.forename: C A
authors.initials: CA
authors.lastname: Pereira
authors.forename: A
authors.initials: A
authors.lastname: Bingen
authors.forename: M
authors.initials: M
authors.lastname: Valle
authors.forename: J P
authors.initials: JP
authors.lastname: Martin
authors.forename: F
authors.initials: F
authors.lastname: Koehren
authors.forename: C
authors.initials: C
authors.lastname: Royer
authors.forename: J L
authors.initials: JL
authors.lastname: Gendrault
authors.forename: A
authors.initials: A
authors.lastname: Kirn
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D018352:Coronavirus Infections / Q000188:drug therapy / Q000276:immunology / Q000473:pathology*; D003571:Cytochalasin B / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000473:pathology*; D006524:Hepatitis, Viral, Animal / Q000188:drug therapy / Q000276:immunology / Q000473:pathology*; D007113:Immunity, Innate / Q000235:genetics; D008099:Liver / Q000098:blood supply*; D051379:Mice; D008805:Mice, Inbred A; D008807:Mice, Inbred BALB C; D008855:Microscopy, Electron, Scanning; D006517:Murine hepatitis virus
chemical_list: D003571:Cytochalasin B