包括一个形成深口袋区域的N-HR衍生肽具有强大的抗HIV-1活性，且对T-20无拮抗作用。
Potent anti-HIV-1 activity of N-HR-derived peptides including a deep pocket-forming region without antagonistic effects on T-20.
作者信息
Izumi Kazuki, Watanabe Kentaro, Oishi Shinya, Fujii Nobutaka, Matsuoka Masao, Sarafianos Stefan G, Kodama Eiichi N
机构信息
Laboratory of Virus Control, Institute for Virus Research, Department of Bioorganic Medical Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
出版信息
Antivir Chem Chemother. 2011 Aug 23;22(1):51-5. doi: 10.3851/IMP1836.
BACKGROUND
Enfuvirtide (T-20), a C-terminal heptad repeat (C-HR)-derived peptide of HIV-1 glycoprotein, gp41, effectively suppresses HIV-1 replication through a putative mechanism that involves it acting as a decoy and binding to the N-terminal heptad repeat (N-HR) of the virus. In this study, we address whether the anti-HIV-1 activity of T-20 is antagonized by a variety of N-HR-derived peptides.
METHODS
Multinuclear activation of galactosidase indicator assays were used to evaluate T-20 activity in the presence of N-HR-derived peptides. The gp41-derived peptides were chemically synthesized.
RESULTS
We demonstrate additive anti-HIV activity when T-20 is used in combination with N-HR-derived peptides that do not have a putative binding region for the tryptophan-rich domain in T-20. The presence of a deep pocket-forming region in the N-HR-derived peptides enhanced their anti-HIV-1 activity, but had little effect on the activity of T-20.
CONCLUSIONS
These results indicate that T-20-based antiviral therapies can be combined with N-HR-derived peptides.
背景
恩夫韦肽（T-20）是一种源自HIV-1糖蛋白gp41 C端七肽重复序列（C-HR）的肽，通过一种假定机制有效抑制HIV-1复制，该机制涉及它作为诱饵与病毒的N端七肽重复序列（N-HR）结合。在本研究中，我们探讨了多种源自N-HR的肽是否会拮抗T-20的抗HIV-1活性。
方法
使用半乳糖苷酶指示剂分析的多核激活来评估在存在源自N-HR的肽的情况下T-20的活性。源自gp41的肽是化学合成的。
结果
我们证明，当T-20与不具有T-20中富含色氨酸结构域假定结合区域的源自N-HR的肽联合使用时，具有相加的抗HIV活性。源自N-HR的肽中存在深口袋形成区域增强了它们的抗HIV-1活性，但对T-20的活性影响很小。
结论
这些结果表明基于T-20的抗病毒疗法可与源自N-HR的肽联合使用。
Zotero 插件