Westmead Millennium Institute, Centre for Virus Research, P.O. Box 412, Westmead, New South Wales, Australia 2145.
J Virol. 2011 Jul;85(14):7465-71. doi: 10.1128/JVI.00088-11. Epub 2011 May 18.
The human cytomegalovirus UL111A gene is expressed during latent and productive infections, and it codes for homologs of interleukin-10 (IL-10). We examined whether viral IL-10 expressed during latency altered differentiation of latently infected myeloid progenitors. In comparison to infection with parental virus or mock infection, latent infection with a virus in which the gene encoding viral IL-10 has been deleted upregulated cytokines associated with dendritic cell (DC) formation and increased the proportion of myeloid DCs. These data demonstrate that viral IL-10 restricts the ability of latently infected myeloid progenitors to differentiate into DCs and identifies an immunomodulatory role for viral IL-10 which may limit the host's ability to clear latent virus.
人类巨细胞病毒 UL111A 基因在潜伏和有性感染期间表达,它编码白细胞介素-10(IL-10)的同源物。我们研究了潜伏期间表达的病毒 IL-10 是否改变了潜伏感染的髓系祖细胞的分化。与亲本病毒感染或模拟感染相比,缺失编码病毒 IL-10 的基因的病毒潜伏感染上调了与树突状细胞(DC)形成相关的细胞因子,并增加了髓样 DC 的比例。这些数据表明,病毒 IL-10 限制了潜伏感染的髓系祖细胞分化为 DC 的能力,并确定了病毒 IL-10 的免疫调节作用,这可能限制了宿主清除潜伏病毒的能力。