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Blocking interactions between HIV-1 integrase and cellular cofactors: an emerging anti-retroviral strategy.

机译:阻断HIV-1整合酶与细胞辅助因子之间的相互作用:一种新兴的抗逆转录病毒策略。

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摘要

HIV-1 integrase (IN) executes the insertion of proviral DNA into the host cell genome, an essential step in the retroviral life cycle. This is a multi-step process that starts in the cytosol and culminates in the nucleus of the infected cell. It is becoming increasingly clear that IN interacts with a wide range of different host-cell proteins throughout the viral life cycle. These cellular cofactors are exploited for various functions, including nuclear import, DNA target-site selection and virion assembly. The disruption of key interactions between IN and direct cellular cofactors affords a novel therapeutic approach for the design and development of new classes of anti-retroviral agents. Here, we will discuss the rationale behind this emerging and promising therapeutic strategy for HIV drug discovery. Our discussion includes the identified IN cellular cofactors, key research developments in the field and the implications this approach will have on the current HIV treatment regimen.
机译:HIV-1整合酶(IN)将前病毒DNA插入宿主细胞基因组,这是逆转录病毒生命周期中的重要步骤。这是一个多步骤过程,始于胞质溶胶,最终达到被感染细胞的细胞核。在病毒的整个生命周期中,IN与多种不同的宿主细胞蛋白相互作用越来越清楚。这些细胞辅因子具有多种功能,包括核输入,DNA靶位选择和病毒体组装。 IN与直接细胞辅因子之间关键相互作用的破坏为新型抗逆转录病毒药物的设计和开发提供了一种新颖的治疗方法。在这里,我们将讨论这种针对HIV药物发现的新兴且有希望的治疗策略背后的原理。我们的讨论包括已确定的IN细胞辅助因子,该领域的关键研究进展以及该方法对当前HIV治疗方案的影响。

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