敖竹君，Kallesh Danappa Jayappa，姚小剑

    (曼尼托巴大学医学院 微生物系人类逆转录病毒实验室，温尼伯 曼尼托巴，加拿大)

    Productive infection of non-dividing cells by HIV-1 requires viral double stranded DNA (dsDNA), which associates with viral and cellular proteins in a large preintegration complex (PIC) to actively enter through the intact nuclear membrane for its integration.Such an active, energy-dependent nuclear import process suggests that HIV-1 employs the cellular nuclear import machinery to accomplish its PIC nuclear import during viral replication[1].At the molecular level, the active nuclear import ability of HIV-1 is attributed to the karyophilic properties of viral PICs.It is known that several viral nucleophilic proteins, including integrase (IN), matrix (p17) and Viral protein R (Vpr), are associated with this nucleoprotein complex and play significant roles in HIV-1 nuclear import[2-7]. Moreover, a unique DNA structure, known as the central DNA flap in viral cDNA, has also been implicated in this viral replication step[8-9]. Interestingly, among them, HIV-1 IN and the central DNA flap collectively contribute to HIV-1 nuclear import not only in non-dividing cells but also in dividing cells[8,10-12].It suggests that the nuclear entry of HIV-1 PICs in dividing cells may not be a passive process.Consistently, it was also reported that the nuclear import of HIV-1 PICs may not rely on mitosis in cycling cells[13]. ......