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紫外线照射的痘苗病毒在正常和着色性干皮病成纤维细胞中的存活情况;紫外线损伤病毒DNA修复的证据

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

作者信息

Klein B, Filon A R, van Zeeland A A, van der Eb A J

机构信息

Laboratory for Molecular Carcinogenesis, Leiden University, The Netherlands.

出版信息

Mutat Res. 1994 May 1;307(1):25-32. doi: 10.1016/0027-5107(94)90274-7.

DOI:10.1016/0027-5107(94)90274-7
PMID:7513804
Abstract

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.

摘要

痘苗病毒可在多种脊椎动物细胞的细胞质中复制,且独立于DNA复制和基因转录所需的大多数或所有细胞酶及因子。为研究痘苗病毒是否也独立于细胞核中存在的核苷酸切除修复酶,我们研究了紫外线照射病毒在正常人成纤维细胞以及来自不同着色性干皮病(XP)互补组(A、C、D、G和XP变异型)的成纤维细胞中的宿主细胞再活化情况。结果发现,紫外线损伤的痘苗病毒在正常细胞和所有测试的紫外线敏感细胞株中的存活率相同,这表明它独立于宿主细胞切除修复酶。这与Lytle等人(1972年)的结果一致,但与Závadová(1971年)的数据相矛盾。在所有测试细胞中,痘苗病毒存活的D37约为7 J/m2,表明在正常细胞中痘苗病毒对紫外线非常敏感。我们还发现,环丁烷嘧啶二聚体从亲本病毒DNA链上消失,这表明痘苗病毒DNA会经历某种形式的DNA修复。文中讨论了这些结果的意义。

相似文献

1
Survival of UV-irradiated vaccinia virus in normal and xeroderma pigmentosum fibroblasts; evidence for repair of UV-damaged viral DNA.紫外线照射的痘苗病毒在正常和着色性干皮病成纤维细胞中的存活情况;紫外线损伤病毒DNA修复的证据
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Carcinogenesis. 1989 Sep;10(9):1691-6. doi: 10.1093/carcin/10.9.1691.
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Host-cell reactivation in mammalian cells. II. Survival of herpes simplex virus and vaccinia virus in normal human and xeroderma pigmentosum cells.
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Comparative study of nucleotide excision repair defects between XPD-mutated fibroblasts derived from trichothiodystrophy and xeroderma pigmentosum patients.毛发硫营养不良和着色性干皮病患者来源的XPD突变成纤维细胞核苷酸切除修复缺陷的比较研究。
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Host-cell reactivation of ultraviolet-irradiated SV40 DNA in five complementation groups of xeroderma pigmentosum.着色性干皮病五个互补组中紫外线照射的SV40 DNA的宿主细胞复活
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J Biol Chem. 1993 Mar 5;268(7):4839-47.

引用本文的文献

1
UV Irradiation of Vaccinia Virus-Infected Cells Impairs Cellular Functions, Introduces Lesions into the Viral Genome, and Uncovers Repair Capabilities for the Viral Replication Machinery.UV 照射感染痘苗病毒的细胞会损害细胞功能,导致病毒基因组出现损伤,并揭示病毒复制机制的修复能力。
J Virol. 2022 May 11;96(9):e0213721. doi: 10.1128/jvi.02137-21. Epub 2022 Apr 11.
2
Mutagenic repair of double-stranded DNA breaks in vaccinia virus genomes requires cellular DNA ligase IV activity in the cytosol.双链 DNA 断裂的诱变修复在痘病毒基因组中需要细胞 DNA 连接酶 IV 在细胞质中的活性。
J Gen Virol. 2018 Jun;99(6):790-804. doi: 10.1099/jgv.0.001034. Epub 2018 Apr 20.
3
Vaccinia virus gene A18R encodes an essential DNA helicase.
痘苗病毒基因A18R编码一种必需的DNA解旋酶。
J Virol. 1995 Oct;69(10):6131-9. doi: 10.1128/JVI.69.10.6131-6139.1995.