Husain Matloob, Moss Bernard
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0445, USA.
J Virol. 2003 Nov;77(21):11754-66. doi: 10.1128/jvi.77.21.11754-11766.2003.
Vaccinia virus assembles two distinct lipoprotein membranes. The primary membrane contains nonglycosylated proteins, appears as crescents in the cytoplasm, and delimits immature and mature intracellular virions. The secondary or wrapping membrane contains glycoproteins, is derived from virus-modified trans-Golgi or endosomal cisternae, forms a loose coat around some intracellular mature virions, and becomes the envelope of extracellular virions. Although the mode of formation of the wrapping membrane is partially understood, we know less about the primary membrane. Recent reports posit that the primary membrane originates from the endoplasmic reticulum-Golgi intermediate compartment (ERGIC). According to this model, viral primary membrane proteins are cotranslationally inserted into the ER and accumulate in the ERGIC. To test the ERGIC model, we employed Sar1(H79G), a dominant negative form of the Sar1 protein, which is an essential component of coatomer protein II (COPII)-mediated cargo transport from the ER to the ERGIC and other post-ER compartments. Overexpression of Sar1(H79G) by transfection or by a novel recombinant vaccinia virus with an inducible Sar1(H79G) gene resulted in retention of ERGIC 53 in the ER but did not interfere with localization of viral primary membrane proteins in factory regions or with formation of viral crescent membranes and infectious intracellular mature virions. Wrapping of intracellular mature virions and formation of extracellular virions did not occur, however, because some proteins that are essential for the secondary membrane were retained in the ER as a consequence of Sar1(H79G) overexpression. Our data argue against an essential role of COPII-mediated cargo transport and the ERGIC in the formation of the viral primary membrane. Instead, viral membranes may be derived directly from the ER or by a novel mechanism.
痘苗病毒组装两种不同的脂蛋白膜。初级膜含有非糖基化蛋白,在细胞质中呈月牙形,界定未成熟和成熟的细胞内病毒粒子。次级膜或包裹膜含有糖蛋白,源自病毒修饰的反式高尔基体或内体囊泡,在一些细胞内成熟病毒粒子周围形成松散的包膜,并成为细胞外病毒粒子的包膜。尽管对包裹膜的形成方式已有部分了解,但我们对初级膜的了解较少。最近的报道认为初级膜起源于内质网-高尔基体中间区室(ERGIC)。根据该模型,病毒初级膜蛋白在共翻译过程中插入内质网并在内质网-高尔基体中间区室积累。为了测试内质网-高尔基体中间区室模型,我们使用了Sar1(H79G),它是Sar1蛋白的显性负性形式,是II型衣被蛋白(COPII)介导的货物从内质网运输到内质网-高尔基体中间区室及其他内质网后区室的重要组成部分。通过转染或携带可诱导Sar1(H79G)基因的新型重组痘苗病毒过表达Sar1(H79G),导致内质网-高尔基体中间区室蛋白53(ERGIC 53)滞留在内质网中,但不干扰病毒初级膜蛋白在工厂区域的定位,也不影响病毒月牙形膜和感染性细胞内成熟病毒粒子的形成。然而,细胞内成熟病毒粒子的包裹和细胞外病毒粒子的形成并未发生,因为由于Sar1(H79G)的过表达,一些对次级膜至关重要的蛋白滞留在了内质网中。我们的数据表明,COPII介导的货物运输和内质网-高尔基体中间区室在病毒初级膜形成过程中并非起关键作用。相反,病毒膜可能直接源自内质网或通过一种新机制形成。