Wang C T, Stegeman-Olsen J, Zhang Y, Barklis E
Vollum Institute for Advanced Biomedical Research, Oregon Health Sciences University, Portland 97201.
Virology. 1994 May 1;200(2):524-34. doi: 10.1006/viro.1994.1215.
We have studied the assembly of human immunodeficiency virus (HIV-1) Gag-B-galactosidase (Gag-B-gal; GBG) fusion proteins into HIV particles in the presence of HIV Gag proteins. Release of fusion proteins from cells was measured by assay of media versus cellular B-gal activities and was dependent on co-expression of unfused Gag proteins. Gag-B-gal incorporation into virus particles was demonstrated by detergent treatment and density gradient fractionation studies and was dependent on protein-protein interactions requiring the C-terminal two-thirds of the HIV CA domain. The central MA domain appeared unimportant for fusion protein incorporation; a nonmyristylated GBG protein was incorporated but at a relatively reduced level, while the NC and p6 domains slightly affected the assembly of fusion proteins into particles. Subcellular fractionation studies showed that all fusion proteins including the nonmyristylated one were enriched in the cytoplasmic pellet fraction. However, assembly into particles did not correlate with subcellular fractionation patterns. Similarly, virion incorporation levels of Gag-B-gal proteins did not correlate with their immunofluorescence localization patterns. However, we observed that while most fusion proteins displayed a perinuclear ring with heterogeneous staining throughout cells, short fusion proteins appeared enriched on the intracellular membranes, and fusion proteins with intact MA but deleted NC domains showed an enhanced surface staining without a clear perinuclear ring. Altogether, our data suggest that the CA domain is the primary determinant for assembly of HIV fusion proteins into virus particles.
我们研究了在存在HIV Gag蛋白的情况下,人类免疫缺陷病毒(HIV-1)Gag-β-半乳糖苷酶(Gag-β-gal;GBG)融合蛋白组装到HIV颗粒中的情况。通过检测培养基与细胞中β-半乳糖苷酶活性来测量融合蛋白从细胞中的释放,其依赖于未融合的Gag蛋白的共表达。通过去污剂处理和密度梯度分级分离研究证明了Gag-β-gal掺入病毒颗粒中,并且依赖于需要HIV CA结构域C末端三分之二的蛋白质-蛋白质相互作用。中央MA结构域对于融合蛋白的掺入似乎不重要;一种非肉豆蔻酰化的GBG蛋白被掺入,但水平相对降低,而NC和p6结构域对融合蛋白组装到颗粒中略有影响。亚细胞分级分离研究表明,所有融合蛋白,包括非肉豆蔻酰化的融合蛋白,都在细胞质沉淀部分中富集。然而,组装到颗粒中与亚细胞分级分离模式无关。同样,Gag-β-gal蛋白的病毒体掺入水平与其免疫荧光定位模式也不相关。然而,我们观察到,虽然大多数融合蛋白在整个细胞中呈现出具有异质性染色的核周环,但短融合蛋白似乎在细胞内膜上富集,并且具有完整MA但缺失NC结构域的融合蛋白显示出增强的表面染色,没有清晰的核周环。总之,我们的数据表明,CA结构域是HIV融合蛋白组装到病毒颗粒中的主要决定因素。