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The emergence of sv 40 variants in a persistent infection of rhesus monkey kidney cells and their interaction with standard sv 40






Virology 95(2): 598-614

The emergence of sv 40 variants in a persistent infection of rhesus monkey kidney cells and their interaction with standard sv 40

In a persistent infection of rhesus monkey kidney cells with SV40, a heterogeneous population of variant particles emerges to replace the large plaque standard SV40 used to initiate the infection. The variants include defective interfering (DI) particles which reach detectable levels at week 6 and which are in excess of plaque forming units (PFU) by week 9. Stocks which contain an excess of DI particle activity contain an excess of particles able to produce T antigen, but not V antigen. Homotypic interference by SV40 DI particles results from a competitive interaction with standard SV40 during replication. Between 7-10 wk of persistent infection, the large-plaque standard SV40 is replaced by infectious small-plaque particles. Between 14-28 wk, the uncloned carrier culture stocks became temperature-sensitive for replication. Restriction endonuclease analysis revealed some changes in carrier culture viral DNA with the first changes evident by week 2. As late as week 57, most of the viral DNA from the carrier system yielded restriction endonuclease fragments indistinguishable from standard virus fragments.

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Accession: 006670883



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