ULTRAVIOLET INACTIVATION OF AVIAN-SARCOMA VIRUSES - BIOLOGICAL AND BIOCHEMICAL-ANALYSIS

The rate of inactivation by UV light of the focus-forming capacity of avian sarcoma virus was almost the same as that of the virus-producing capacity, measured as plaque formation. No significant difference was observed in inactivation of the transforming capacity assayed on C/BE chick embryo fibroblasts (CEF), which carry endogenous avian tumor virus DNA, and on duck embryo fibroblasts (DEF), which are devoid of this DNA. All foci induced by nonirradiated virus produced infectious sarcoma virus, but some of the foci induced by UV-irradiated virus did not produce infectious virus of either transforming or transformation-defective type. The proportion of nonproducer foci was 3.4 times more in DEF than in gs- chf- CEF. RNAs extracted from UV-irradiated virions by sodium dodecyl sulfate (SDS) treatment were found to be composed of 60-70 S and 4 S RNAs by analysis in a sucrose gradient containing 0.5% SDS. The large RNA became hydrophobic after irradiation and was sedimented with SDS by addition of 1 drop of saturated potassium chloride solution. This RNA was not dissociated into 30-40 S components by heating at 100.degree. C for 45 s, unlike 60-70 S RNA from unirradiated virions. After SDS-Pronase treatment, the 60-70 S RNA from UV-irradiated virions no longer had these altered characteristics. Reverse transcriptase activity with the endogenous template decreased in parallel with increase in the UV dose. The reduction rate was similar to that assayed with exogenous template or in the presence of actinomycin D. RNA damage may not be the only cause of virus inactivation by UV light.