Goh Gerard Kian-Meng, Dunker A Keith, Uversky Vladimir N
Center for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Virol J. 2008 Oct 23;5:126. doi: 10.1186/1743-422X-5-126.
A previous study (Goh G.K.-M., Dunker A.K., Uversky V.N. (2008) Protein intrinsic disorder toolbox for comparative analysis of viral proteins. BMC Genomics. 9 (Suppl. 2), S4) revealed that HIV matrix protein p17 possesses especially high levels of predicted intrinsic disorder (PID). In this study, we analyzed the PID patterns in matrix proteins of viruses related and unrelated to HIV-1.
Both SIVmac and HIV-1 p17 proteins were predicted by PONDR VLXT to be highly disordered with subtle differences containing 50% and 60% disordered residues, respectively. SIVmac is very closely related to HIV-2. A specific region that is predicted to be disordered in HIV-1 is missing in SIVmac. The distributions of PID patterns seem to differ in SIVmac and HIV-1 p17 proteins. A high level of PID for the matrix does not seem to be mandatory for retroviruses, since Equine Infectious Anemia Virus (EIAV), an HIV cousin, has been predicted to have low PID level for the matrix; i.e. its matrix protein p15 contains only 21% PID residues. Surprisingly, the PID percentage and the pattern of predicted disorder distribution for p15 resemble those of the influenza matrix protein M1 (25%).
Our data might have important implications in the search for HIV vaccines since disorder in the matrix protein might provide a mechanism for immune evasion.
先前的一项研究(Goh G.K.-M., Dunker A.K., Uversky V.N.(2008年)用于病毒蛋白比较分析的蛋白质内在无序工具箱。BMC基因组学。9(增刊2),S4)表明,HIV基质蛋白p17具有特别高的预测内在无序水平(PID)。在本研究中,我们分析了与HIV-1相关和不相关的病毒基质蛋白中的PID模式。
PONDR VLXT预测SIVmac和HIV-1 p17蛋白均高度无序,存在细微差异,分别含有50%和60%的无序残基。SIVmac与HIV-2密切相关。在SIVmac中缺少一个在HIV-1中预测为无序的特定区域。SIVmac和HIV-1 p17蛋白中PID模式的分布似乎有所不同。对于逆转录病毒来说,基质高水平的PID似乎并非必需,因为与HIV亲缘关系较近的马传染性贫血病毒(EIAV)的基质蛋白预测具有低PID水平;即其基质蛋白p15仅含有21%的PID残基。令人惊讶的是,p15的PID百分比和预测的无序分布模式与流感基质蛋白M1(25%)相似。
我们的数据可能对寻找HIV疫苗具有重要意义,因为基质蛋白的无序可能提供一种免疫逃逸机制。