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作 者:施先宗[1,2] 王珣章[1,2] 龙綮新[1,2] 吴文言[1,2] 李迎秋[1,2] 曲士芮 陈曲侯[1,2]
机构地区:[1]中山大学昆虫学研究所 [2]华中师范大学昆虫研究所
出 处:《病毒学报》1999年第1期78-83,共6页Chinese Journal of Virology
基 金:国家自然科学基金
摘 要:细胞凋亡(Apoptosis)或细胞程序性死亡(Programmedceldeath,PCD),最早被定义为一种有秩序、受控制并按某种预定程序发展的生理性自然死亡过程〔1〕。诱导细胞发生凋亡的因素很多,而病毒感染是常见的导致细胞凋亡的重要因素之一。由...An extra copy of p35 (p35 ORF and p35 EPO ) gene was introduced into the genome of TnNPV in order to show their effects on very late gene expression. The p35 ORF and p35 EPO fragments were oriented directly under the control of the synthetic and XIV promoters in the transfer vector pSXIVVI +X3. Two strategies were followed to construct the p35 directly oriented recombinant TnNPVs (TnNPV Δp10/LacZ + ΔHBVS/polh ++p35 ORF and TnNPV Δp10/LacZ +-ΔHBV S/polh ++p35 EPO )either by inserting lacZ gene first into the viral genome or by inserting directly oriented p35 first. The cells infected with TnNPV Δp10/lacZ + ΔHBV S/polh ++p35 ORF or TnNPV Δp10/lacZ +-ΔHBV S/polh ++p35 EPO showed no significant differences in their survival ratios at the end of infection. The recombinant viruses produced less β galactosidase activities than the control did, and the virus with early and late overexpression of p35 produced the least β galactosidase. The result was comparable to that of the virus production. Obviously, overexpression of p35 late or early and late affected TnNPV late and very late gene expression. Both of them suggested that p35 does play a role in normal viral replication.
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