INDUCTION OF THYMIDINE KINASE-ACTIVITY BY VIRUSES WITH GROUP-B DNA GENOMES - BOVINE CYTOMEGALOVIRUS (BOVINE HERPESVIRUS-4)

被引:53
作者
KIT, S
KIT, M
ICHIMURA, H
CRANDELL, R
MCCONNELL, S
机构
[1] BAYLOR COLL MED, HOUSTON, TX 77030 USA
[2] TEXAS A&M UNIV, DEPT VET MICROBIOL & PARASITOL, COLLEGE STN, TX 77843 USA
[3] TEXAS A&M UNIV, TEXAS VET MED DIAGNOST LAB, COLLEGE STN, TX 77843 USA
关键词
D O I
10.1016/0168-1702(86)90041-9
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The bovine herpesvirus type 4 (BHV-4) group has a slow replication cycle, a narrow host range, and cytopathogenic effects characteristic of cytomegaloviruses (CMV), but a Group B genome structure similar to that of lymphotropic Herpesvirus saimiri (HVS). Reference BHV-4 strain DN599 and BHV-4 strains N124 and FHV-2 induced in the cytosol fraction of thymidine kinase-negative (TK-) rabbit skin (RAB-BU) cell mutants a novel TK activity. The BHV-4-induced thymidine kinase (TK) differed from the principal cytosol TK of mock-infected cells in PAGE mobility (Rm) under non-denaturing conditions and in the capacity to efficiently substitute CTP for ATP as a phosphate donor. The BHV-4 thymidine phosphorylating activity could also be distinguished from many common herpesvirus-induced TKs because it lacked iododeoxycytidine phosphorylating activity. Iododeoxyuridine, trifluorothymidine and bromovinyldeoxyuridine inhibited [3H]thymidine (0.01 mM) phosphorylation by the BHV-4 enzyme in a dose-dependent manner, but arabinosylthymine and 2''-fluoro-5-methyl-arabinosyluracil (FMAU) were poor inhibitors of [3H]thymidine phosphorylation, and acyclovir and (dihydroxy-2-propoxymethyl)guanine (DHPG) did not inhibit at all at 60 and 40 times the concentrations of [3H]thymidine, respectively.
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页码:197 / 212
页数:16
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