Modification of Epstein-Barr virus replication by tunicamycin.
The effect of tunicamycin, which inhibits N-linked glycosylation, on the replication of Epstein-Barr virus was examined. Tunicamycin markedly reduced the yield of virus from producing cells. At concentrations of 1 to 2 micrograms of tunicamycin per ml, there was a buildup of intracellular virus in P3HR1-Cl13 cells but not in MCUV5 cells; at a concentration of 5 micrograms of tunicamycin per ml in P3HR1-Cl13 cells, viral DNA synthesis was inhibited as well. Viral glycoproteins lacking N-linked sugars were apparently inserted into the cell membrane, and the small amount of virus made in the presence of drug was able to bind specifically to its receptor on B cells. However, the ability of the virus to induce immunoglobulin secretion by fresh human lymphocytes was impaired. This implies a role for viral glycoproteins in the penetration as well as the attachment of virus.
D000818:Animals; D000914:Antibodies, Viral / Q000096:biosynthesis; D000956:Antigens, Viral / Q000032:analysis; D002143:Callitrichinae; D002460:Cell Line; D004261:DNA Replication / Q000187:drug effects; D005944:Glucosamine / Q000031:analogs & derivatives*; D006023:Glycoproteins / Q000096:biosynthesis; D004854:Herpesvirus 4, Human / Q000187:drug effects* / Q000276:immunology / Q000502:physiology; D006801:Humans; D008214:Lymphocytes / Q000382:microbiology; D008565:Membrane Proteins / Q000096:biosynthesis; D009844:Oligosaccharides / Q000378:metabolism; D011499:Protein Processing, Post-Translational / Q000187:drug effects; D011991:Receptors, Virus / Q000378:metabolism; D014415:Tunicamycin / Q000494:pharmacology*; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication / Q000187:drug effects*
D000914:Antibodies, Viral; D000956:Antigens, Viral; D006023:Glycoproteins; D008565:Membrane Proteins; D009844:Oligosaccharides; D011991:Receptors, Virus; D014764:Viral Proteins; D014415:Tunicamycin; D005944:Glucosamine