Vpr-induced cell cycle arrest is conserved among primate lentiviruses
Vpr-induced cell cycle arrest is conserved among primate lentiviruses
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DOI：
10.1128/jvi.70.4.2516-2524.1996
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发表时间：
1996-04-01
影响因子：
5.4
通讯作者：
Chen, ISY
中科院分区：
文献类型：
--
作者：
Planelles, V;Jowett, JBM;Chen, ISY
我们先前报道了人类免疫缺陷病毒1型毒株NL 4 -3（HIV-1（NL 4 -3））vpr的表达导致细胞停滞在细胞周期的G（2）期。我们研究了其他HIV-1分离株和HIV-1以外的灵长类慢病毒对细胞周期阻滞的诱导作用。我们证明，vpr基因从组织培养适应或原代分离的HIV-1能够诱导G（2）停滞。此外，我们证明，诱导细胞周期阻滞是一个保守的功能的成员的其他两组灵长类慢病毒，HIV-2/猿猴免疫缺陷病毒株SM（SIVsm）/SIVmac和SIVagm，vpr从HIV-1，HIV-2，和SIVmac诱导细胞周期阻滞时，转染人（HeLA）和猴（CV-1）细胞。来自HIV-2和SIVmac的vpx在两种细胞类型中均未诱导可检测的细胞周期停滞，并且SIVagm vpx能够诱导CV-1细胞而非HeLa细胞的细胞周期停滞。这些结果表明，诱导细胞周期扰动是感染灵长类动物的慢病毒的一般特性。这种病毒功能在整个进化过程中的保守性表明，它在病毒-宿主关系中起着关键作用，阐明其机制可能揭示灵长类慢病毒诱导的病理学的重要线索。
We previously reported that expression of human immunodeficiency virus type 1 strain NL4-3 (HIV-1(NL4-3)) vpr causes cells to arrest in the G(2) phase of the cell cycle. We examined the induction of cell cycle arrest by other HIV-1 isolates and by primate lentiviruses other than HIV-1. We demonstrate that the vpr genes from tissue culture-adapted or primary isolates of HIV-1 are capable of inducing G(2) arrest. In addition, we demonstrate that induction of cell cycle arrest is a conserved function of members of two other groups of primate lentiviruses, HIV-2/simian immunodeficiency virus strain sm (SIVsm)/SIVmac and SIVagm, vpr from HIV-1, HIV-2, and SIVmac induced cell cycle arrest when transfected in human (HeLA) and monkey (CV-1) cells. vpx from HIV-2 and SIVmac did not induce detectable cell cycles arrest in either cell type, and SIVagm vpx was capable of inducing arrest in CV-1 but not HeLa cells. These results indicate that induction of cell cycle perturbation is a general property of lentiviruses that infect primates. The conservation of this viral function throughout evolution suggests that it plays a key role in virus-host relationships, and elucidation of its mechanism may reveal important clues about pathology induced by primate lentiviruses.