monensin and Herpes-Simplex

The effects of tunicamycin and monensin on the morphogenesis of herpes simplex virus type 1 and on the ultrastructure and function of host cell membranes was investigated by conventional technics of electron microscopy and cytochemical localization of glycoproteins with thiocarbohydrazide-SO2. Infected RS 537 rabbit fibroblasts were treated with tunicamycin, which inhibits the glycosylation of many glycoproteins, or monensin, which inhibits the transport of proteins to the cell surface, and were compared with untreated infected cells. Tunicamycin treatment almost entirely suppresses the perinuclear envelopment of viral capsids, induces the nuclear export of unusually numerous naked viral capsids, and prevents the proliferation of the Golgi apparatus. On the other hand, perinuclear envelopment of viral capsids still occurs following a monensin treatment; however, enveloped viral capsids are not released into the extracellular space; in addition this treatment induces the proliferation of the rough endoplasmic reticulum (RER). The number of structures stained for glycoproteins in tunicamycin-treated cells is markedly lower than that in nontreated infected cells, whereas an unusual additional staining of the entire outer nuclear membrane and of the RER occurs following monensin treatment.

Topics: Animals; Cells, Cultured; Fibroblasts; Herpes Simplex; Membrane Glycoproteins; Monensin; Rabbits; Tunicamycin