Mulky Alok, Sarafianos Stefan G, Arnold Edward, Wu Xiaoyun, Kappes John C
Department of Microbiology, University of Alabama at Birmingham, 35294, USA.
J Virol. 2004 Jul;78(13):7089-96. doi: 10.1128/JVI.78.13.7089-7096.2004.
The human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) is a heterodimer comprised of two structurally distinct subunits (p51 and p66). Since p51 and p66 are derived from the same coding region, subunit-specific structure-function studies of RT have been conducted exclusively by in vitro biochemical approaches. To study RT subunit function in the context of infectious virus, we constructed an LTR-vpr-p51-IRES-p66 expression cassette in which the HIV-1 vpr gene was fused in frame with p51, followed by an internal ribosome entry site (IRES) sequence and the p66 coding region. By coexpression with RT-deficient proviral DNA, we demonstrated that the p66 subunit is specifically and selectively packaged into virions as a Vpr-p51/p66 complex. Our analysis showed that cleavage by the viral protease liberates Vpr and generates functional heterodimeric RT (p51/p66) that supports HIV-1 reverse transcription and virus infection. By exploiting this novel trans-complementation approach, we demonstrated, for the first time with infectious virions, that the YMDD aspartates of p66 are both required and sufficient for RT polymerase function. Mutational analyses of the p51 YMDD aspartates indicated that they play an important structural role in p51 folding and subunit interactions that are required for the formation of an active RT heterodimer within infected cells. Understanding the role of the individual RT subunits in RNA- and DNA-dependent DNA synthesis is integral to our understanding of RT function. Our findings will lead to important new insights into the role of the p51 and p66 subunits in HIV-1 reverse transcription.
人类免疫缺陷病毒1型(HIV-1)逆转录酶(RT)是一种由两个结构不同的亚基(p51和p66)组成的异二聚体。由于p51和p66来自相同的编码区域,RT亚基特异性的结构-功能研究一直仅通过体外生化方法进行。为了在感染性病毒的背景下研究RT亚基的功能,我们构建了一个LTR-vpr-p51-IRES-p66表达盒,其中HIV-1 vpr基因与p51读框融合,随后是一个内部核糖体进入位点(IRES)序列和p66编码区。通过与缺乏RT的前病毒DNA共表达,我们证明p66亚基作为Vpr-p51/p66复合物被特异性且选择性地包装到病毒粒子中。我们的分析表明,病毒蛋白酶的切割释放出Vpr并产生功能性异二聚体RT(p51/p66),其支持HIV-1逆转录和病毒感染。通过利用这种新型的反式互补方法,我们首次在感染性病毒粒子中证明,p66的YMDD天冬氨酸对于RT聚合酶功能既是必需的也是足够的。对p51 YMDD天冬氨酸的突变分析表明,它们在p51折叠以及在受感染细胞内形成活性RT异二聚体所需的亚基相互作用中发挥重要的结构作用。了解各个RT亚基在依赖RNA和DNA的DNA合成中的作用对于我们理解RT功能至关重要。我们的发现将为p51和p66亚基在HIV-1逆转录中的作用带来重要的新见解。