中文摘要：

尽管 HIV-1 子类型 B 仍然在发达国家统治流行爱滋病，在开发国家的越来越多的人正在受不了非子类型 B 病毒的流行病。什么是更坏的， antiretroviral 药的 combinational 使用的功效被药抵抗的快速的发展逐渐地损害。获得卓见进药抵抗， 10-ns MD 模拟同时与 4 不同朊酶( B wt ， B 傻瓜， F wt 和 F 傻瓜)在 TL-3 禁止者的建筑群上被进行，在哪个之中有 TL-3 禁止者的 B wt 朊酶的建筑群被当作控制组。 MD 数据的详细分析显示对 TL-3 的 B 傻瓜的药抵抗主要源于一张重要的氢契约的损失并且 F ， wt 被恐水病的相互作用的减少在 S1/S1 引起衣袋，当两上面提及的二个原因是 F 傻瓜朊酶抵抗的原因时。这些结果在对以前的实验的好同意，揭示为对 TL-3 禁止者的上述的朊酶子类型的药抵抗的可能的机制。另外，另一个指示被获得 M36I， V82A 和 L90M 的变化可以导致结构的变换以便改变禁止者绑定模式。

英文摘要：

Although HIV-1 subtype B still dominates the epidemic AIDS in developed countries, an increasing number of people in devel- oping countries are suffering from an epidemic of non-subtype B viruses. What is worse, the efficacy of the combinational use of antiretroviral drugs is gradually compromised by the rapid development of drug resistance. To gain an insight into drug resistance, 10-ns MD simulations were simultaneously conducted on the complexes of the TL-3 inhibitor with 4 different proteases （Bwt, Bmut, Fwt and Fmut）, among which the complex of the Bwt protease with the TL-3 inhibitor was treated as the control group. Detailed analyses of MD data indicated that the drug resistance of Bmut against TL-3 mainly derived from loss of an important hydrogen bond and that of Fwt was caused by the decrease of hydrophobic interactions in S 1/S 1＇ pocket, while both of the two reasons mentioned above were the cause of the Fmut protease＇s resistance. These results are in good agreement with the previous experiments, revealing a possible mechanism of drug resistance for the aforementioned protease subtypes against the TL-3 inhibitor. Additionally, another indication was obtained that the mutations of M36I, V82A and L90M may induce structural transforms so as to alter the inhibitor＇s binding mode.