Survival of UV-irradiated vaccinia virus in normal and xeroderma pigmentosum fibroblasts; evidence for repair of UV-damaged viral DNA.

Vaccinia virus replicates in the cytoplasm of cells from a large number of vertebrates and is independent of most or all cellular enzymes and factors needed for DNA replication and gene transcription. To investigate whether vaccinia virus is also independent of nucleotide excision-repair enzymes present in the nucleus, we have investigated the host-cell reactivation of UV-irradiated virus in normal human fibroblasts and fibroblasts from various xeroderma pigmentosum (XP) complementation groups (A, C, D, G and XP-variant). It was found that the survival of UV-damaged vaccinia virus is the same in the normal and all UV-sensitive cell strains tested, suggesting it is independent of host-cell excision-repair enzymes. This agrees with results of Lytle et al. (1972), but is in conflict with data from Závadová (1971). The D37 of vaccinia virus survival is approximately 7 J/m2 in all cells tested, indicating that in normal cells vaccinia virus is very sensitive to ultraviolet light. We also found that cyclobutane pyrimidine dimers disappear from parental viral DNA strands, suggesting that vaccinia DNA is subject to some form of DNA repair. The implications of these results are discussed.