Bego Mariana G, Dubé Mathieu, Mercier Johanne, Cohen Eric A
Laboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal, 110, Avenue des Pins Ouest, Montreal, Quebec, Canada H2W 1R7.
J Virol. 2009 Dec;83(24):13032-6. doi: 10.1128/JVI.01786-09. Epub 2009 Sep 30.
The human immunodeficiency virus type 1 (HIV-1) accessory protein Vpu enhances virus particle release by counteracting a host factor that retains virions at the surfaces of infected cells. It was recently demonstrated that cellular protein BST-2/CD317/Tetherin restricts HIV-1 release in a Vpu-dependent manner. Calcium-modulating cyclophilin ligand (CAML) was also proposed to be involved in this process. We investigated whether CAML is involved in cell surface expression of Tetherin. Here, we show that CAML overexpression in permissive Cos-7 cells or CAML depletion in restrictive HeLa cells has no effect on HIV-1 release or on Tetherin surface expression, indicating that CAML is not required for Tetherin-mediated restriction of HIV-1 release.
1型人类免疫缺陷病毒(HIV-1)辅助蛋白Vpu通过对抗一种将病毒粒子滞留在受感染细胞表面的宿主因子来增强病毒粒子的释放。最近有研究表明,细胞蛋白BST-2/CD317/栓系蛋白以Vpu依赖的方式限制HIV-1的释放。钙调节亲环素配体(CAML)也被认为参与了这一过程。我们研究了CAML是否参与栓系蛋白的细胞表面表达。在此,我们发现,在允许性的Cos-7细胞中过表达CAML或在限制性的HeLa细胞中耗尽CAML,对HIV-1的释放或栓系蛋白的表面表达均无影响,这表明CAML并非栓系蛋白介导的HIV-1释放限制所必需的。