Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
J Mol Biol. 2011 Sep 23;412(3):354-64. doi: 10.1016/j.jmb.2011.07.055. Epub 2011 Jul 29.
Steps in the replication of human immunodeficiency virus type 1 (HIV-1) occurring in the virus but not in the host are preferred targets of antiretroviral therapy. Strand transfer is unique; the DNA strand being made by viral reverse transcriptase (RT) is moved from one RNA template position to another. Understanding the mechanism requires knowing whether the RT directly mediates the template exchange or dissociates during the exchange, so that it occurs by polymer dynamics. Earlier work in vitro showed that the presence of an RT-trapping polymer would allow synthesis on the original or donor template but completely block transfer and subsequent synthesis on the second or acceptor template. One interpretation is that the RT must dissociate during transfer, but an alternative is that sequestration of non-polymerizing RTs prevents polymerization-independent ribonuclease H (RNase H) cleavages of the donor template necessary for strand exchange. To resolve this ambiguity, we designed a primer-template system that allows strand transfer without RNase H activity. Using an RNase H negative mutant RT, we showed that a polymer trap still prevented strand transfer. This confirms that RT dissociates during strand transfer. The presence of HIV-1 nucleocapsid protein, which promotes strand exchange, had little effect on this outcome. Additional assays showed that both the wild-type RT and a multiple nucleoside RT inhibitor-resistant HIV-1 RT containing an extended fingers domain, which is characterized by its enhanced primer-template binding affinity, were unable to transfer with the trapping polymer. This implies that common sequence variations among RTs are unlikely to alter dissociation feature.
人类免疫缺陷病毒 1 型(HIV-1)的复制步骤发生在病毒中而不是宿主中,是抗逆转录病毒治疗的首选靶点。链转移是独特的;由病毒逆转录酶(RT)制成的 DNA 链从一个 RNA 模板位置移动到另一个位置。了解该机制需要知道 RT 是否直接介导模板交换,或者在交换过程中解离,从而通过聚合物动力学发生交换。早期的体外研究表明,RT 捕获聚合物的存在将允许在原始或供体模板上进行合成,但完全阻止转移和随后在第二个或受体模板上的合成。一种解释是 RT 必须在转移过程中解离,但另一种解释是未聚合 RT 的隔离阻止了聚合无关的核糖核酸酶 H(RNase H)对供体模板的切割,这种切割对于链交换是必要的。为了解决这个问题,我们设计了一个引物-模板系统,允许在没有 RNase H 活性的情况下进行链转移。使用 RNase H 阴性突变 RT,我们表明聚合物陷阱仍然阻止了链转移。这证实了 RT 在链转移过程中解离。促进链交换的 HIV-1 核衣壳蛋白的存在对这一结果几乎没有影响。其他测定表明,野生型 RT 和一种包含扩展手指结构域的多核苷酸 RT 抑制剂耐药 HIV-1 RT(其特征是增强的引物-模板结合亲和力)都无法与捕获聚合物一起转移。这意味着 RT 之间常见的序列变异不太可能改变解离特征。