Allison Steven L, Tao Yizhi J, O'Riordain Gabriel, Mandl Christian W, Harrison Stephen C, Heinz Franz X
Institute of Virology, University of Vienna, A-1095 Vienna, Austria.
J Virol. 2003 Nov;77(21):11357-66. doi: 10.1128/jvi.77.21.11357-11366.2003.
Flaviviruses assemble in the endoplasmic reticulum by a mechanism that appears to be driven by lateral interactions between heterodimers of the envelope glycoproteins E and prM. Immature intracellular virus particles are then transported through the secretory pathway and converted to their mature form by cleavage of the prM protein by the cellular protease furin. Earlier studies showed that when the prM and E proteins of tick-borne encephalitis virus are expressed together in mammalian cells, they assemble into membrane-containing, icosahedrally symmetrical recombinant subviral particles (RSPs), which are smaller than whole virions but retain functional properties and undergo cleavage maturation, yielding a mature form in which the E proteins are arranged in a regular T = 1 icosahedral lattice. In this study, we generated immature subviral particles by mutation of the furin recognition site in prM. The mutation resulted in the secretion of two distinct size classes of particles that could be separated by sucrose gradient centrifugation. Electron microscopy showed that the smaller particles were approximately the same size as the previously described mature RSPs, whereas the larger particles were approximately the same size as the virus. Particles of the larger size class were also detected with a wild-type construct that allowed prM cleavage, although in this case the smaller size class was far more prevalent. Subtle differences in endoglycosidase sensitivity patterns suggested that, in contrast to the small particles, the E glycoproteins in the large subviral particles and whole virions might be in nonequivalent structural environments during intracellular transport, with a portion of them inaccessible to cellular glycan processing enzymes. These proteins thus appear to have the intrinsic ability to form alternative assembly products that could provide important clues about the role of lateral envelope protein interactions in flavivirus assembly.
黄病毒在内质网中通过一种似乎由包膜糖蛋白E和prM异二聚体之间的侧向相互作用驱动的机制进行组装。未成熟的细胞内病毒颗粒随后通过分泌途径运输,并通过细胞蛋白酶弗林蛋白酶切割prM蛋白转化为成熟形式。早期研究表明,当蜱传脑炎病毒的prM和E蛋白在哺乳动物细胞中共同表达时,它们组装成含膜的、二十面体对称的重组亚病毒颗粒(RSPs),其比完整病毒体小,但保留功能特性并经历切割成熟,产生一种成熟形式,其中E蛋白以规则的T = 1二十面体晶格排列。在本研究中,我们通过突变prM中的弗林蛋白酶识别位点产生了未成熟的亚病毒颗粒。该突变导致分泌出两种不同大小类别的颗粒,可通过蔗糖梯度离心分离。电子显微镜显示,较小的颗粒与先前描述的成熟RSPs大小大致相同,而较大的颗粒与病毒大小大致相同。用允许prM切割的野生型构建体也检测到了较大尺寸类别的颗粒,尽管在这种情况下较小尺寸类别更为普遍。内切糖苷酶敏感性模式的细微差异表明,与小颗粒不同,大的亚病毒颗粒和完整病毒体中的E糖蛋白在细胞内运输过程中可能处于不等价的结构环境中,其中一部分对细胞聚糖加工酶不可及。因此,这些蛋白似乎具有形成替代组装产物的内在能力,这可能为包膜蛋白侧向相互作用在黄病毒组装中的作用提供重要线索。