Gudima Severin, Chang Jinhong, Moraleda Gloria, Azvolinsky Anna, Taylor John
Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111-2497, USA.
J Virol. 2002 Apr;76(8):3709-19. doi: 10.1128/jvi.76.8.3709-3719.2002.
Assembly of hepatitis delta virus (HDV) in infected human hepatocytes involves association of the 1,679- nucleotide single-stranded genomic RNA (deltaRNA) with multiple copies of both small and large forms of the delta protein (deltaAg) to form a ribonucleoprotein particle which in turn interacts with envelope proteins of the natural helper virus, hepatitis B virus. Subsequently, for initiation of a new round of replication, the amount of small deltaAg within the assembled HDV particle is both necessary and sufficient. Quantitative assays were used in order to better understand just how much deltaAg is needed. The molar ratio of deltaAg species to genomic deltaRNA in assembled HDV particles was approximately 200. Next, this ratio was determined for cells under several different experimental situations in which HDV genome replication was occurring. These included replication in woodchuck liver and also in mouse liver and skeletal muscle, as well as replication in stably and transiently transfected cultured human hepatoblastoma cells. Surprisingly, in almost all these situations the molar ratios were comparable to that observed for HDV particles. This was true for different times after the initiation of replication and was independent of whether or not virus assembly was occurring. Cell fractionation combined with quantitative assays was used to test whether the majority of deltaAg and deltaRNA were colocalized during HDV replication in transfected cells. The cytoplasmic fraction contained the majority of deltaAg and genomic deltaRNA. Finally, the quality of deltaAg and deltaRNA, especially at relatively late times after the initiation of replication, was examined by using reverse transcription-PCR, cloning, and sequencing through the entire deltaAg open reading frame. When virus assembly and spread were not possible, 20% or less of the predicted deltaAg would have been able to support HDV replication. In summary, an examination of the quantity, quality and intracellular distribution of deltaAg and deltaRNA in several different experimental systems has provided a better understanding of the parameters associated with the initiation, maintenance, and ultimate decline of HDV genome replication.
丁型肝炎病毒(HDV)在受感染的人类肝细胞中的组装过程包括1679个核苷酸的单链基因组RNA(δRNA)与小、大两种形式的δ蛋白(δAg)的多个拷贝相结合,形成核糖核蛋白颗粒,该颗粒进而与天然辅助病毒乙型肝炎病毒的包膜蛋白相互作用。随后,为启动新一轮复制,组装好的HDV颗粒内小δAg的量是必需且足够的。为了更好地了解需要多少δAg,我们进行了定量分析。组装好的HDV颗粒中δAg种类与基因组δRNA的摩尔比约为200。接下来,在几种不同的HDV基因组正在复制的实验情况下,测定了细胞中的这个比例。这些情况包括在土拨鼠肝脏、小鼠肝脏和骨骼肌中的复制,以及在稳定和瞬时转染的培养人肝癌细胞中的复制。令人惊讶的是,在几乎所有这些情况下,摩尔比都与在HDV颗粒中观察到的相当。这在复制开始后的不同时间都是如此,并且与病毒组装是否发生无关。细胞分级分离结合定量分析用于测试在转染细胞中HDV复制期间大多数δAg和δRNA是否共定位。细胞质部分含有大部分δAg和基因组δRNA。最后,通过使用逆转录PCR、克隆以及对整个δAg开放阅读框进行测序,检查了δAg和δRNA的质量,特别是在复制开始后相对较晚的时间。当病毒组装和传播不可能时,预测的δAg的20%或更少将能够支持HDV复制。总之,对几种不同实验系统中δAg和δRNA的数量、质量和细胞内分布的研究,使我们对与HDV基因组复制的起始、维持和最终下降相关的参数有了更好的理解。