|
pubmed:abstractText |
At low multiplicities of infection (1 to 5 PFU/cell), human adenoviruses grew inefficiently in monkey kidney cells as the result of a late transcriptional and/or translational defect. Through an unknown mechanism, coinfection with simian virus 40 (SV40) could overcome this block. Coincident with the onset of adenovirus DNA replication in coinfected monkey cells, however, there was a marked inhibition of SV40 DNA replication. Since this inhibition in SV40 DNA synthesis occurred in the presence of normal SV40 transcription and protein synthesis, we suggest that adenovirus competes with SV40 for molecules specifically required for DNA synthesis (e.g., SV40 T-antigen). At high multiplicities of adenovirus infection (50 PFU/cell), adenoviruses could grow efficiently in monkey kidney cells. In cells coinfected under these conditions, SV40 transcription was generally inhibited, as shown by a decrease in nuclear and cytoplasmic SV40 mRNA.
|
