We have used a non-replicating recombinant adenovirus, Ad5MCMVlacZ, which 
expresses the beta-galactosidase reporter gene, to examine both constitutive and 
inducible repair of UV-damaged DNA in repair proficient CHO-AA8 Chinese hamster 
ovary cells and in mutant CHO-UV61 cells which are deficient in the 
transcription-coupled repair (TCR) pathway of nucleotide excision repair. Host 
cell reactivation (HCR) of beta-galactosidase activity for UV-irradiated 
Ad5MCMVlacZ was significantly reduced in non-irradiated CHO-UV61 cells compared 
to that in non-irradiated CHO-AA8 cells suggesting that repair in the 
transcribed strand of the UV-damaged reporter gene in untreated cells utilizes 
TCR. Prior UV-irradiation of cells with low UV fluences resulted in a transient 
enhancement of HCR for expression of the UV-damaged reporter gene in CHO-AA8 
cells but not in TCR deficient CHO-UV61 cells. These results suggest the 
presence of an inducible DNA pathway in CHO cells that results from an 
enhancement of TCR or a mechanism that involves the TCR pathway.