I may have misunderstood something but I thought that all homologous recombination events depend on an initial step of MRN/ATM.
Many Ad vectors are Ad5 based which contains an E4Orf3 which mislocalizes components of MRN complex to avoid DDR mechanisms. If this is true, and DDR and HR are completely nonfunctional during Ad infection, how can first generation Ad5 viral vectors recombine with the E1 locus in HEK293 to form replication competent Ad??