Fouchier R A, Malim M H
Howard Hughes Medical Institute, University of Pennsylvania School of Medicine, Philadelphia 19104-6148, USA.
Adv Virus Res. 1999;52:275-99. doi: 10.1016/s0065-3527(08)60302-4.
Following infection-mediated entry into the cytoplasm, retroviral cores form large nucleoprotein complexes (PICs) which undergo reverse transcription and, ultimately, catalyze provirus formation. The ability of these complexes to be specifically imported into the nucleus via NPCs explains why nondividing cells can be productively infected with lentiviruses such as HIV-1, whereas productive infection by the oncoretrovirus MLV is restricted to proliferating cells. Current evidence suggests that virally encoded protein components of the HIV-1 PIC, in particular IN and Vpr, act in concert to target these complexes for nuclear import by recruiting cellular import factors and interacting with the NPCs. Here have we reviewed recent advances made in this complex and fascinating area of HIV-1 biology and have discussed them in relation to models for postentry nuclear import in other retroviral and nonretroviral systems.
在感染介导进入细胞质后,逆转录病毒核心形成大型核蛋白复合物(PICs),这些复合物进行逆转录,并最终催化前病毒的形成。这些复合物通过核孔复合体(NPCs)特异性导入细胞核的能力解释了为什么非分裂细胞能够被诸如HIV-1等慢病毒有效感染,而致肿瘤逆转录病毒MLV的有效感染则局限于增殖细胞。目前的证据表明,HIV-1 PIC的病毒编码蛋白成分,特别是整合酶(IN)和病毒蛋白R(Vpr),通过招募细胞导入因子并与NPCs相互作用,协同作用将这些复合物靶向导入细胞核。在此,我们综述了HIV-1生物学这一复杂而迷人领域的最新进展,并结合其他逆转录病毒和非逆转录病毒系统中进入后核导入的模型进行了讨论。