Inhibition of DNA replication of adenovirus type 5 and simian virus 40 by tunicamycin.

Addition of tunicamycin, a glycosylation inhibitor, to SV40-infected CV-1 cells or Ad5-infected HeLa cells at the beginning of infection was found to inhibit the accumulation of viral DNA at late times after infection. However, tunicamycin did not block viral DNA replication when added to the infected cells at late times after infection. The inhibitory effect of tunicamycin was partially reversible in the presence of acetylglucosamine, suggesting that the effect was due to glycosylation. In spite of diminished amounts of viral DNA accumulated at the late phase of infection in the presence of tunicamycin, the transcription rate of Ad5 late RNA and the amount of adenovirus late proteins and mRNA were not significantly affected by tunicamycin treatment. The inhibitory effect of tunicamycin on Ad5 DNA replication was much reduced in 293 cells which provide E1a gene products in trans. Similar observation was obtained for the replication of SV40 DNA in Cos-7 cells which provide SV40 early gene products in trans. These results suggest that tunicamycin inhibits a glycosylation event induced by the early gene products of Ad5 and SV40 viruses during the early phase of infection.