This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Türler, H Articles by Salomon, C Search for Related Content PubMed PubMed Citation Articles by Türler, H Articles by Salomon, C

 Previous Article  |  Next Article 

J Virol. 1985 February; 53(2): 579-586

Small and middle T antigens contribute to lytic and abortive polyomavirus infection.

ABSTRACT

Using three different polyomavirus hr-t mutants and two polyomavirus mlT mutants, we studied induction of S-phase by mutants and wild-type virus in quiescent mouse kidney cells, mouse 3T6 cells, and FR 3T3 cells. At different times after infection, we measured the proportion of T-antigen-positive cells, the incorporation of [3H]thymidine, the proportion of DNA-synthesizing cells, and the increase in total DNA, RNA, and protein content of the cultures. In permissive mouse cells, we also determined the amount of viral DNA and the proportion of viral capsid-producing cells. In polyomavirus hr-t mutant-infected cultures, onset of host DNA replication was delayed by several hours, and a smaller proportion of T-antigen-positive cells entered S-phase than in wild-type-infected cultures. Of the two polyomavirus mlT mutants studied, dl-23 behaved similarly to wild-type virus in many, but not all, parameters tested. The poorly replicating but well-transforming mutant dl-8 was able to induce S-phase, and (in permissive cells) progeny virus production, in only about one-third of the T-antigen-positive cells. From our experiments, we conclude that mutations affecting small and middle T-antigen cause a reduction in the proportion of cells responding to virus infection and a prolongation of the early phase, i.e., the period before cells enter S-phase. In hr-t mutant-infected mouse 3T6 cells, production of viral DNA was less than 10% of that in wild-type-infected cultures; low hr-t progeny production in 3T6 cells was therefore largely due to poor viral DNA replication.

This article has been cited by other articles:

• Chen, L., Wang, X., Fluck, M. M. (2006). Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication.. J. Virol. 80: 7295-7307 [Abstract] [Full Text]  
• Chen, L., Fluck, M. M. (2001). Role of Middle T-Small T in the Lytic Cycle of Polyomavirus: Control of the Early-to-Late Transcriptional Switch and Viral DNA Replication. J. Virol. 75: 8380-8389 [Abstract] [Full Text]  
• Gottlieb, K. A., Villarreal, L. P. (2001). Natural Biology of Polyomavirus Middle T Antigen. Microbiol. Mol. Biol. Rev. 65: 288-318 [Abstract] [Full Text]