Institute for Molecular Virology and McArdle Laboratory for Cancer Research University of Wisconsin-Madison, 1525 Linden Drive, Madison, WI, 53706, USA.
Institute for Molecular Virology and McArdle Laboratory for Cancer Research University of Wisconsin-Madison, 1525 Linden Drive, Madison, WI, 53706, USA.
Virus Res. 2019 Sep;270:197646. doi: 10.1016/j.virusres.2019.197646. Epub 2019 Jun 28.
Human cytomegalovirus (HCMV) establishes latency within incompletely differentiated cells of the myeloid lineage. The viral protein UL138 participates in establishing and maintaining this latent state. UL138 has multiple functions during latency that include silencing productive phase viral gene transcription and modulating intracellular protein trafficking. Trafficking and subsequent downregulation of the multidrug resistance-associated protein 1 (MRP1) by UL138 is mediated by one of four Golgi sorting motifs within UL138. Here we investigate whether any of the Golgi sorting motifs of UL138 are required for the establishment and/or maintenance of HCMV latency in model cell systems in vitro. We determined that a mutant UL138 protein lacking an acidic cluster dileucine sorting motif unable to downregulate MRP1, as well as another mutant lacking all four Golgi sorting motifs still silenced viral immediate early (IE) gene expression and prevented progeny virion formation during latency. We conclude that the Golgi sorting motifs are not required for latency establishment or maintenance in model cell systems in vitro.
人巨细胞病毒(HCMV)在未完全分化的髓系细胞中建立潜伏状态。病毒蛋白 UL138 参与建立和维持这种潜伏状态。UL138 在潜伏期间具有多种功能,包括沉默有性相病毒基因转录和调节细胞内蛋白质运输。UL138 通过 UL138 内的四个高尔基体分拣基序之一来介导多药耐药相关蛋白 1(MRP1)的运输和随后的下调。在这里,我们研究了 UL138 的任何高尔基体分拣基序是否需要在体外模型细胞系统中建立和/或维持 HCMV 潜伏。我们确定,一种缺乏酸性簇二亮氨酸分拣基序的突变 UL138 蛋白无法下调 MRP1,另一种缺乏所有四个高尔基体分拣基序的突变体仍然沉默病毒即刻早期(IE)基因表达,并在潜伏期间阻止子代病毒粒子形成。我们得出结论,高尔基体分拣基序不是体外模型细胞系统中潜伏建立或维持所必需的。