Zhang W H, Hockley D J, Nermut M V, Morikawa Y, Jones I M
Institute of Virology, Oxford, UK.
J Gen Virol. 1996 Apr;77 ( Pt 4):743-51. doi: 10.1099/0022-1317-77-4-743.
Seven internal deletions within the p24 domain of the human immunodeficiency virus type 1 Gag precursor have been assessed for their effect on Gag particle formation following their expression using recombinant baculoviruses. In addition, each deleted molecule was assessed for its ability to bind soluble p24 antigen in vitro. The mutants fell into three different phenotypic groups: (i) three mutants that had no effect on either p24 binding or Gag particle assembly, (ii) three mutants that abolished both features and (iii) one mutant that bound p24 in vitro but failed to assemble particles. Mutations that abolished both in vitro p24 binding and particle assembly mapped to the C terminus of p24 confirming this region as critical for virion assembly. We suggest the division of virion assembly into at least two distinct phases and suggest a model in which the critical sequences mapped to date are combined with available structural information.
利用重组杆状病毒表达人类免疫缺陷病毒1型Gag前体的p24结构域内的7个内部缺失，评估了它们对Gag颗粒形成的影响。此外，还评估了每个缺失分子在体外结合可溶性p24抗原的能力。这些突变体分为三个不同的表型组：(i) 三个对p24结合或Gag颗粒组装均无影响的突变体；(ii) 三个消除了这两个特征的突变体；(iii) 一个在体外能结合p24但无法组装颗粒的突变体。消除体外p24结合和颗粒组装的突变定位到p24的C末端，证实该区域对病毒体组装至关重要。我们建议将病毒体组装至少分为两个不同阶段，并提出一个模型，其中迄今定位的关键序列与现有的结构信息相结合。
