Cobbold C, Wileman T
Division of Immunology, Institute for Animal Health, Pirbright Laboratory, Surrey, England.
J Virol. 1998 Jun;72(6):5215-23. doi: 10.1128/JVI.72.6.5215-5223.1998.
African swine fever virus (ASFV) is a large enveloped DNA virus that shares the striking icosahedral symmetry of iridoviruses. To understand the mechanism of assembly of ASFV, we have been studying the biosynthesis and subcellular distribution of p73, the major structural protein of ASFV. Sucrose density sedimentation of lysates prepared from infected cells showed that newly synthesized p73 was incorporated into a complex with a size of 150 to 250 kDa. p73 synthesized by in vitro translation migrated at 70 kDa, suggesting that cellular and/or viral proteins are required for the formation of the 150- to 250-kDa complex. During a 2-h chase, approximately 50% of the newly synthesized pool of p73 bound to the endoplasmic reticulum (ER). During this period, the membrane-bound pool of p73, but not the cytosolic pool, formed large complexes of approximately 50,000 kDa. The complexes were formed via assembly intermediates, and the entire membrane-associated pool of p73 was incorporated into the 50,000-kDa complex within 2 h. The 50,000-kDa complexes containing p73 were also detected in virions secreted from cells. Immunoprecipitation of sucrose gradients with sera taken from hyperimmune pigs suggested that p73 was the major component of the 50,000-kDa complex. It is possible, therefore, that the complex contains between 600 and 700 copies of p73. The kinetics of complex formation and envelopment of p73 were similar, and complex formation and envelopment were both reversibly inhibited by cycloheximide, suggesting a functional link between complex assembly and ASFV envelopment. A protease protection assay detected 50,000-kDa complexes on the inside and outside of the membranes forming the viral envelope. The identification of a complex containing p73 beneath the envelope of ASFV suggests that p73 may be a component of the inner core shell or matrix of ASFV. The outer pool may represent p73 within the outer capsid layer of the virus. In summary, the data suggest that the assembly of the inner core matrix and outer capsid of ASFV takes place on the ER membrane during envelopment and that these structures are not preassembled in the cytosol.
非洲猪瘟病毒(ASFV)是一种大型包膜DNA病毒,具有与虹彩病毒惊人的二十面体对称性。为了解ASFV的组装机制,我们一直在研究ASFV的主要结构蛋白p73的生物合成和亚细胞分布。对感染细胞制备的裂解物进行蔗糖密度沉降分析表明,新合成的p73被整合到一个大小为150至250 kDa的复合物中。体外翻译合成的p73迁移率为70 kDa,这表明150至250 kDa复合物的形成需要细胞和/或病毒蛋白。在2小时的追踪过程中,新合成的p73池中约50%与内质网(ER)结合。在此期间,与膜结合的p73池而非胞质池形成了约50,000 kDa的大复合物。这些复合物通过组装中间体形成,并且在2小时内,整个与膜相关的p73池都被整合到50,000 kDa的复合物中。从超免疫猪采集的血清对蔗糖梯度进行免疫沉淀表明,p73是50,000 kDa复合物的主要成分。因此,该复合物可能包含600至700个p73拷贝。p73复合物形成和包膜化的动力学相似,并且复合物形成和包膜化均被环己酰亚胺可逆抑制,这表明复合物组装与ASFV包膜化之间存在功能联系。蛋白酶保护试验在形成病毒包膜的膜的内侧和外侧检测到50,000 kDa的复合物。在ASFV包膜下方鉴定出含有p73的复合物表明,p73可能是ASFV内核壳或基质的组成部分。外部池可能代表病毒外衣壳层内的p73。总之,数据表明ASFV内核基质和外衣壳的组装在包膜化过程中发生在内质网膜上,并且这些结构并非在细胞质中预先组装。