University of Cambridge, Department of Medicine, Box 157, Level 5 Laboratories Block, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
J Gen Virol. 2011 Jul;92(Pt 7):1539-1549. doi: 10.1099/vir.0.031377-0. Epub 2011 Apr 6.
One site of latency of human cytomegalovirus (HCMV; human herpesvirus 5) is known to be CD34(+) haematopoietic progenitor cells, and it is likely that carriage of latent virus has profound effects on cellular gene expression in order to optimize latency and reactivation. As microRNAs (miRNAs) play important roles in regulating stem-cell gene expression, this study asked whether latent carriage of HCMV led to changes in cellular miRNA expression. A comprehensive miRNA screen showed the differential regulation of a number of cellular miRNAs during HCMV latency in CD34(+) progenitor cells. One of these, hsa-miR-92a, was robustly decreased in three independent miRNA screens. Latency-induced change in hsa-miR-92a results in an increase in expression of GATA-2 and subsequent increased expression of cellular IL-10, which aids the maintenance of latent viral genomes in CD34(+) cells, probably resulting from their increased survival.
人类巨细胞病毒 (HCMV; 人类疱疹病毒 5) 的一个潜伏部位已知是 CD34(+)造血祖细胞,为了优化潜伏和激活,潜伏病毒的携带很可能对细胞基因表达产生深远影响。由于 microRNAs (miRNAs) 在调节干细胞基因表达方面发挥着重要作用,本研究探讨了 HCMV 的潜伏携带是否导致细胞 miRNA 表达发生变化。全面的 miRNA 筛选显示,在 CD34(+)祖细胞中 HCMV 潜伏时,许多细胞 miRNA 的表达受到差异调控。其中之一,hsa-miR-92a,在三个独立的 miRNA 筛选中均显著下调。hsa-miR-92a 的潜伏诱导变化导致 GATA-2 的表达增加,随后细胞内 IL-10 的表达增加,这有助于 CD34(+)细胞中潜伏病毒基因组的维持,可能是由于它们的存活率增加。