Interferon (α, β and γ) susceptibility was tested in a human cell line, UV-1, a u.v. light-resistant variant of RSa cells; the latter have high sensitivity to both u.v. lethality and the cell profileration inhibition (anticellular) effect of human interferon (HuIFN) preparations. UV-1 cells were less sensitive than the parental RSa cells to the inhibitory effects of HuIFN preparations, as measured by cell proliferation and the incorporation of [H]deoxythymidine and [H]deoxyadenosine into acid-insoluble cellular material. Nevertheless, UV-1 cells exposed to HuIFN showed almost the same enhanced levels of antiviral activity and pppA(2′p5′A) synthetase activity as similarly treated RSa cells. Further, UV-1 cells had much the same binding capacity for I-labelled HuIFN-αA. Thus, it seems likely that the variant has an increased resistance to the anticellular effect but not to the antiviral effect of HuIFN preparations. UV-1 cells showed no significant difference from RSa cells in u.v.-induced DNA repair synthesis. However, when a comparison was made between the susceptibility of normal fibroblasts and fibroblasts from patients with Cockayne's syndrome, characterized by an altered u.v. sensitivity but no alteration of DNA repair replication synthesis, the Cockayne's syndrome fibroblasts, CCK-3 and CCK-4, were more susceptible to HuIFN-β as judged by cell proliferation and deoxythymidine incorporation tests.


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