Hussain Mazhar, Asgari Sassan
School of Integrative Biology, University of Queensland, St. Lucia, QLD 4072, Australia.
Apoptosis. 2008 Dec;13(12):1417-26. doi: 10.1007/s10495-008-0268-8.
Ascoviruses (AVs) induce a unique pathology in their insect host cells causing cleavage of the cells into virion-containing vesicles. The mechanism by which AVs induce vesicle formation is poorly understood. It is postulated that the virus initially induces apoptosis leading to cell fragmentation. The apoptotic bodies are however, rescued by the virus to form the vesicles. Here we show that Heliothis virescens AV (HvAV-3e) is able to inhibit chemically induced apoptosis from around 16 h after infection. Analysis of the genome of the virus indicated the presence of a putative inhibitor of apoptosis (orf28) gene that encodes a protein with an imperfect baculovirus inhibitor of apoptosis repeat (BIR) and a RING domain. Transiently expressed orf28 did not inhibit chemically induced apoptosis suggesting that the protein may not serve as an inhibitor of apoptosis. Nevertheless, RNA interference studies revealed that the gene is probably essential for virus pathology and replication.
ascoviruses（AVs）在其昆虫宿主细胞中引发独特的病理变化，导致细胞裂解成含有病毒粒子的囊泡。人们对AVs诱导囊泡形成的机制了解甚少。据推测，病毒最初诱导细胞凋亡导致细胞破碎。然而，凋亡小体被病毒拯救以形成囊泡。在这里，我们表明棉铃虫AV（HvAV-3e）能够在感染后约16小时左右抑制化学诱导的细胞凋亡。对病毒基因组的分析表明存在一个假定的凋亡抑制因子（orf28）基因，该基因编码一种具有不完美杆状病毒凋亡抑制重复序列（BIR）和一个RING结构域的蛋白质。瞬时表达的orf28并不抑制化学诱导的细胞凋亡，这表明该蛋白质可能不作为凋亡抑制因子。然而，RNA干扰研究表明该基因可能对病毒病理和复制至关重要。
