Höglund S, Ohagen A, Lawrence K, Gabuzda D
Department of Biochemistry, HIV Structure Group, Biomedical Center, Uppsala, Sweden.
Virology. 1994 Jun;201(2):349-55. doi: 10.1006/viro.1994.1300.
The viral infectivity factor gene vif of human immunodeficiency virus type 1 (HIV-1) has been shown to enhance the cell-free infectivity of HIV-1 virus particles. Previous studies have demonstrated that vif increases viral infectivity at the time of virus production, most likely by affecting viral protein processing, virus assembly, or virus maturation. The effect of vif on the assembly and maturation of HIV-1 propagated in CEM, Jurkat, and SupT1 cells was examined by electron microscopy and goniometer analysis. CEM and Jurkat cells are nonpermissive and partially permissive for the replication of vif--defective viruses, respectively, while SupT1 cells are completely permissive. In CEM and Jurkat cultures, the morphology of immature vif+ and vif- virions was similar but immature virus particles were observed at a slightly higher frequency in cultures infected with the vif- virus. At later stages of virus maturation, however, nonhomogeneous packing of the core was detected in the majority of vif- virus particles produced in CEM and Jurkat cells. In the absence of vif, the cone-shaped virus core contained dense material in its broad end but, in contrast to vif+ virions, the material inside its narrow end appeared transparent. The narrow part of the vif- virus core was surrounded by a shell and was attached to the viral envelope by a core-envelope link structure. Vif- virus particles with a lateral body of core material adjacent to the viral envelope were also observed more frequently in CEM and Jurkat cultures. In contrast, in SupT1 cultures the morphology of mature vif+ and vif- virus particles was similar. These results suggest that vif is associated with an effect during the final stages of packing of the viral nucleoprotein core. This effect may be important for the infectivity of HIV-1 virus particles.
人类免疫缺陷病毒1型（HIV-1）的病毒感染性因子基因vif已被证明可增强HIV-1病毒颗粒的无细胞感染性。先前的研究表明，vif在病毒产生时增加病毒感染性，很可能是通过影响病毒蛋白加工、病毒组装或病毒成熟来实现的。通过电子显微镜和测角仪分析，研究了vif对在CEM、Jurkat和SupT1细胞中增殖的HIV-1组装和成熟的影响。CEM和Jurkat细胞分别对vif缺陷病毒的复制不允许和部分允许，而SupT1细胞则完全允许。在CEM和Jurkat培养物中，未成熟的vif+和vif-病毒体的形态相似，但在感染vif-病毒的培养物中观察到未成熟病毒颗粒的频率略高。然而，在病毒成熟的后期阶段，在CEM和Jurkat细胞产生的大多数vif-病毒颗粒中检测到核心的不均匀包装。在没有vif的情况下，锥形病毒核心在其宽端含有致密物质，但与vif+病毒体相比，其窄端内部的物质显得透明。vif-病毒核心的窄部分被一个壳包围，并通过核心-包膜连接结构附着在病毒包膜上。在CEM和Jurkat培养物中也更频繁地观察到具有与病毒包膜相邻的核心物质侧体的vif-病毒颗粒。相比之下，在SupT1培养物中，成熟的vif+和vif-病毒颗粒的形态相似。这些结果表明，vif与病毒核蛋白核心包装的最后阶段的一种效应有关。这种效应可能对HIV-1病毒颗粒的感染性很重要。
