Host factors involved in natural HIV resistance

为了找到新的治疗艾滋病/HIV感染的靶点，我们详细分析了HIV限制性因子trim5 α抗病毒活性的分子机制。我们能够得到以下结果：1。原位脱膜实验表明，HIV-1突变株在猴TRIM5alpha存在下可以复制，脱膜过程延迟。2. 在人trim5 α连接区（coil -coil和SPRY区域之间）天然存在的单氨基酸取代影响其抗hiv -1活性。3. TRIM5alpha可能通过其SPRY区与tlr4介导的信号转导通路中的TAB2结合。

In order to identify novel therapeutic target(s) for AIDS/HIV-infection, we have analyzed detailed molecular mechanisms of anti-viral activity of HIV restriction factor TRIM5alpha. We were able to obtain following results: 1.In situ uncoating assay revealed that an HIV-1 mutant strain, which could replicate in the presence of monkey TRIM5alpha, showed delayed uncoating process. 2. A naturally occurring single amino acid substitution in human TRIM5alpha linker region between coiled-coil and SPRY regions affects its anti-HIV-1 activity. 3. TRIM5alpha could bind to TAB2, which is in the TLR4-mediated signal transduction pathway, probably through its SPRY region.