Loss of surface fibronectin after infection of cultured cells by HSV-1 and 2.
Fibronectin is lost from the surface of HSV infected cells during cell rounding. In order to investigate also the fate of fibronectin during the process of HSV-induced cell-fusion, BHK, Vero as well as primary or secondary rabbit kidney cells were infected with HSV-1 strains producing cell-fusion. By immunofluorescence and immunoelectron microscopy a considerable loss of fibronectin after HSV infection could be demonstrated leaving only irregular clumps of fibronectin containing virus particles on the cell surface. Decrease and disarrangement of fibronectin was similar during cell rounding and cell fusion. Loss of Fibronectin was closely connected with the two types of the cytopathic effect (CPE) and could not be prevented by protease inhibitors. The immediate-early protein 175K is essential for induction of CPE and loss of fibronectin. The damage to the cell membrane during HSV infection shows certain analogous mechanisms with events induced by Cytochalasin B and might be explained by the loss of hypothetical fibronectin receptors.
D008841:Actin Cytoskeleton / Q000648:ultrastructure; D000818:Animals; D002459:Cell Fusion; D002478:Cells, Cultured; D006224:Cricetinae; D003571:Cytochalasin B / Q000494:pharmacology; D005353:Fibronectins / Q000032:analysis*; D006561:Herpes Simplex / Q000378:metabolism / Q000473:pathology; D007668:Kidney; D011480:Protease Inhibitors / Q000494:pharmacology; D011817:Rabbits; D018139:Simplexvirus / Q000254:growth & development*; D014779:Virus Replication
D005353:Fibronectins; D011480:Protease Inhibitors; D003571:Cytochalasin B