## Abstract Amplification of SV40 genes in SV40βtransformed Chinese hamster embryo cells (CO631) by chemical carcinogens as well as by herpes simplex virus infection can be inhibited by infection with the defective parvovirus, AAVβ5. This is shown by __in situ__ hybridization with SV40 DNA of AAVβ5
Repair of psoralen-induced crosslinks in cells multiply infected with SV40
β Scribed by Hall, Jennifer Dean
- Book ID
- 104726591
- Publisher
- Springer
- Year
- 1982
- Tongue
- English
- Weight
- 417 KB
- Volume
- 188
- Category
- Article
- ISSN
- 0026-8925
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β¦ Synopsis
Experiments were conducted to study the relationship between the production of interstrand crosslinks by 4,5',8-trimethylpsoralen (psoralen) in simian virus 40 DNA and the ability of psoralen to inactivate the virus. Under conditions where only single viral particles enter a given host cell, approximately one crosslink was lethal to the virus and could not be repaired. In contrast, when multiple viral genomes infected a host cell, psoralen-induced crosslinks were repaired (multiplicity reactivation). A model is proposed for multiplicity reactivation which involves genetic recombination between damaged viral genomes.
π SIMILAR VOLUMES
Simian virus 40 (SV40) infection of quiescent monkey kidney cells stimulates two successive rounds of cellular DNA synthesis without an intervening mitosis. This uncoupling of S phase and mitosis indicates that SV40 modulates pathways regulating the G2to-M phase transition. To examine the integrity