摘要
苜蓿银纹夜蛾核多角体病毒(Autographa californica multicapsid nuclear polyhedrosis virus,AcMNPV)能够抑制棉铃虫核多角体病毒(Helicoverpa armigera Nucleopoly hedrovirus,HaSNPV)诱导的Tn Hi5 细胞凋亡,并能辅助HaSNPV在Tn Hi5细胞中复制,产生具有感染能力的子代病毒。瞬时表达实验证明,在Tn Hi5细胞中,p35具有明显抑制凋亡的能力,但是不能辅助HaSNPV在Tn Hi5细胞中的复制;进一步构建超表达p35 的重组病毒:vHap35,发现vHap35能够抑制Tn Hi5细胞凋亡,但是不能产生具有感染力的病毒粒子。电镜观察发现感染重组病毒的部分细胞中存在单粒包埋的病毒粒子(ODV)。
Autographa californica multicapsid nucleopolyhedrovirus(AcMNPV) blocked the Tn-Hi5 cell apoptosis stimulated by Helicoverpa armigera nucleopolyhedrovirus (HaSNPV). Futhermore AcMNPV could rescued HaSNPV replication in Tn-Hi5 cell and produced infective virus. This means that HaSNPV extend the host rang with AcMNPV help. The transient expression assay indicated that Ac-p35 could significantly inhibit the Tn-Hi5 apoptosis induced by HaSNPV.A recombinant HaSNPV which overexpression of p35: vHap35, was constructed to futher analyse P35 function. vHap35 was used to infect Tn-Hi5 as we expected the Tn-hi5 cell did not undergo apoptosis. Anyhow, no infective virus BV was detected. Under the electronic microscope viral particles were observed, which probably are the ODVs. The results demonstrat that p35 is funtional as both apoptosis inhibitor and host range factor.
出处
《中国病毒学》
CSCD
2005年第2期173-178,共6页
Virologica Sinica
基金
国家自然科学基金(30325002)
国家973项目(2003CB114202)
