Abstract
Summary 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.