MOUSE HEPATITIS-VIRUS TYPE-3 INFECTION PROVOKES A DECREASE IN THE NUMBER OF SINUSOIDAL ENDOTHELIAL-CELL FENESTRAE BOTH IN-VIVO AND IN-VITRO

Fenestrations of hepatic endothelial cells play an active role as a si eving barrier allowing extensive exchange between the blood and liver parenchyma, Alteration of these structures may be induced in the cours e of various pathological events and provoke important perturbations o f Liver function. We demonstrate here that sinusoidal endothelial cell s are permissive for mouse hepatitis virus 3 (MHV3) in vivo and in vit ro and that this infection leads to a striking decrease in the number of fenestrae, The disappearance of these structures observed under sca nning electron microscopy or in cryofracture preparations in vivo and in vitro cannot be reversed by the action of cytochalasin B on the mic rofilament network. The decrease in the porosity seems to be related d irectly to the productive infection of the endothelial cells, because it was not observed in A/J mice resistant to the virus and in suscepti ble BALB/c mice immunized with a thermosensitive mutant in which no vi ral replication occurs. In conclusion, a viral infection of Liver endo thelial cells may cause extensive loss of the fenestrations and thus l ead to important functional pertubations.