Effect of tunicamycin on the morphogenesis of Semliki Forest Virus and Rous sarcoma virus

Abstract

Semliki Forst Virus (SFV) infected chick embroyo cells (CEC) incubated in the presence of Tunicamyein, a drug which specifically inhibits glycosylation, were studied under the electron microscope. No extracellular virions were produced although intracellular viral nucleocapsids in paracrystalline form were detected. Under these conditions the structures, referred to as type 1 and 2 cytopathic vacuoles (cpv-1 and cpv-2, respectively) as well as membraneous spherules at the plasma membrane could still be observed. CEC rpoductively infected and transformed by Rous sarcoma virus (RSV) incubated for 24 hours in the presence of Tunicamycin (1 microgram/ml) still showed budding and extracellular parties. Intracellur nucleocapsid could could not be detected.

Glycoproteins of Bovine Viral Diarrhoea-Mucosal Disease Virus in Infected Bovine Cells

“…The effect of tunicamycin on the replication of most enveloped virus genera has been reported. It causes profound inhibitory effects on the assembly and morphogenesis of virions as well as on the infectivity of the virions if they are released at all (Gibson et al, 1978 ;Leavitt et ct/., 1977;Ogura et al, 1977;Pizer et al, 1980;Sabara et al, 1982;Schwarz et al, 1976;Stallcup & Fields, 1981 ;Stohrer & Hunter, 1979).…”

Antiviral activity of tunicamycin on herpes simplex virus

“…The effect of tunicamycin on cells infected with various RNA-containing enveloped viruses is essentially similar for all the viruses tested so far. There is a reduction in the infectivity of the virus and interference in the synthesis of the glycopeptides (10,15,17,20 (10,20). With regard to vesicular stomatitis virus, it was mainly attributed to the change in the confonnation and solubility of protein G (10,11).…”

“…Changes in the cell morphology and in the membrane properties of normal and virus-transformed fibroblasts occur in the presence of tunicamycin (3, 4). Tunicamycin significantly lowers the yield of several enveloped ribonucleic acid (RNA)-containing viruses (10,15,17,20). Whereas formation of virions of Semliki Forest, fowl plague (20), Sindbis, and vesicular stomatitis viruses (10) is greatly inhibited by tunicamycin, formation of Rous sarcoma and influenza virions occurs in the presence of the antibiotic; however, these virus particles show reduced infectivity and undetectable amounts of glycoproteins (15,20).…”

Populations of herpes simplex virus glycoprotein gC with and without affinity for the N-acetyl-galactosamine specific lectin ofHelix pomatia

“…All known glycoproteins of enveloped viruses contain high mannose or complex type ohgosaccharides linked to the polypeptide via an N-glycosidic linkage between asparagine and N-aeetylglueosamine (GlcNAc) (6). Under conditions of tunicamyein (TM) inhibition of gtycosylation in virus-infected cells, aberrant polypeptides will be formed resulting in loss of viral infectivity (9,10,16,17,18,25). According to prevailing concepts, the main function of N-glycosidic oligosaecharides is to stabilize the polypeptide conformation and the loss of infectivity is caused only indirectly by the absence of oligosaccharides due to such secondary events as increased sensitivity to intracellutar proteolytic degradation or unspecific aggregation of underglycosylated viral glycoproteins (4).…”