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针对HIV-1蛋白酶抑制剂的耐药途径的贝叶斯网络分析。

Bayesian network analysis of resistance pathways against HIV-1 protease inhibitors.

作者信息

Deforche K, Camacho R, Grossman Z, Silander T, Soares M A, Moreau Y, Shafer R W, Van Laethem K, Carvalho A P, Wynhoven B, Cane P, Snoeck J, Clarke J, Sirivichayakul S, Ariyoshi K, Holguin A, Rudich H, Rodrigues R, Bouzas M B, Cahn P, Brigido L F, Soriano V, Sugiura W, Phanuphak P, Morris L, Weber J, Pillay D, Tanuri A, Harrigan P R, Shapiro J M, Katzenstein D A, Kantor R, Vandamme A-M

机构信息

Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium.

出版信息

Infect Genet Evol. 2007 Jun;7(3):382-90. doi: 10.1016/j.meegid.2006.09.004. Epub 2006 Nov 28.

Abstract

Interpretation of Human Immunodeficiency Virus 1 (HIV-1) genotypic drug resistance is still a major challenge in the follow-up of antiviral therapy in infected patients. Because of the high degree of HIV-1 natural variation, complex interactions and stochastic behaviour of evolution, the role of resistance mutations is in many cases not well understood. Using Bayesian network learning of HIV-1 sequence data from diverse subtypes (A, B, C, F and G), we could determine the specific role of many resistance mutations against the protease inhibitors (PIs) nelfinavir (NFV), indinavir (IDV), and saquinavir (SQV). Such networks visualize relationships between treatment, selection of resistance mutations and presence of polymorphisms in a graphical way. The analysis identified 30N, 88S, and 90M for nelfinavir, 90M for saquinavir, and 82A/T and 46I/L for indinavir as most probable major resistance mutations. Moreover we found striking similarities for the role of many mutations against all of these drugs. For example, for all three inhibitors, we found that the novel mutation 89I was minor and associated with mutations at positions 90 and 71. Bayesian network learning provides an autonomous method to gain insight in the role of resistance mutations and the influence of HIV-1 natural variation. We successfully applied the method to three protease inhibitors. The analysis shows differences with current knowledge especially concerning resistance development in several non-B subtypes.

摘要

在感染患者的抗病毒治疗随访中,对人类免疫缺陷病毒1型(HIV-1)基因型耐药性的解读仍是一项重大挑战。由于HIV-1自然变异程度高、进化过程中存在复杂的相互作用和随机行为,耐药突变在许多情况下的作用尚未得到充分理解。通过对来自不同亚型(A、B、C、F和G)的HIV-1序列数据进行贝叶斯网络学习,我们能够确定许多耐药突变针对蛋白酶抑制剂奈非那韦(NFV)、茚地那韦(IDV)和沙奎那韦(SQV)的具体作用。此类网络以图形方式直观呈现治疗、耐药突变选择和多态性存在之间的关系。分析确定奈非那韦的30N、88S和90M、沙奎那韦的90M以及茚地那韦的82A/T和46I/L为最可能的主要耐药突变。此外,我们发现许多针对所有这些药物的突变作用存在显著相似性。例如,对于所有三种抑制剂,我们发现新突变89I是次要的,且与90位和71位的突变相关。贝叶斯网络学习提供了一种自主方法,以深入了解耐药突变的作用以及HIV-1自然变异的影响。我们成功将该方法应用于三种蛋白酶抑制剂。分析显示与当前知识存在差异,尤其是在几种非B亚型的耐药性发展方面。

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