Sakuma T
Antimicrob Agents Chemother. 1984 Jun;25(6):742-6. doi: 10.1128/AAC.25.6.742.
Strains of varicella-zoster virus resistant to 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil (BV-araU) were isolated from varicella-zoster virus-infected Vero cells which were pulse-treated with 5-iododeoxyuridine or 5-bromodeoxyuridine or both and then treated with BV-araU. These BV-araU-resistant strains (BV-araUr) could not be isolated from varicella-zoster virus-infected cells treated with BV-araU alone and had reduced viral thymidine kinase activity. Two of five BV-araUr strains were also resistant to 5-iododeoxyuridine and 5-bromodeoxyuridine, whereas other BV-araUr strains were relatively susceptible to these drugs. All clones from the BV-araUr strain were susceptible to 1-beta-D-arabinofuranosylcytosine and phosphonoacetic acid, but 7 of 10 clones from the BV-araUr strain were resistant to 1-beta-D-arabinofuranosyladenine. The possible mechanisms of induction of BV-araU resistance are discussed.
从水痘带状疱疹病毒感染的Vero细胞中分离出对1-β-D-阿拉伯呋喃糖基-E-5-(2-溴乙烯基)尿嘧啶(BV-araU)耐药的水痘带状疱疹病毒毒株,这些细胞先用5-碘脱氧尿苷或5-溴脱氧尿苷或两者进行脉冲处理,然后用BV-araU处理。这些对BV-araU耐药的毒株(BV-araUr)无法从仅用BV-araU处理的水痘带状疱疹病毒感染细胞中分离出来,并且其病毒胸苷激酶活性降低。五个BV-araUr毒株中有两个也对5-碘脱氧尿苷和5-溴脱氧尿苷耐药,而其他BV-araUr毒株对这些药物相对敏感。来自BV-araUr毒株的所有克隆对1-β-D-阿拉伯呋喃糖基胞嘧啶和膦甲酸敏感,但来自BV-araUr毒株的10个克隆中有7个对1-β-D-阿拉伯呋喃糖基腺嘌呤耐药。本文讨论了诱导BV-araU耐药的可能机制。