Grupo de Transdução de Sinal, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, 31270-901 Belo Horizonte, Minas, Brazil.
Laboratório de Vírus, Department of Microbiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, 31270-901 Belo Horizonte, Minas Gerais, Brazil.
Viruses. 2018 Mar 21;10(4):140. doi: 10.3390/v10040140.
Evolution has equipped poxvirus genomes with the coding capacity for several virus-host interaction products which interfere with host cell gene expression and protein function, creating an adequate intracellular environment for a productive infection. We show here that (VACV) induces the expression of the cellular transcription factor EGR-1 (early growth response-1) in Mouse Embryonic Fibroblasts (MEFs) through the MEK (mitogen-activated protein kinase (MAPK)/ERK)/ERK (extracellular signal-regulated kinases) pathway, from 3 to 12 h post infection (h.p.i.). By using starved knockout () MEFs, we demonstrate that VACV replication is reduced by ~1 log in this cell line. Although western blotting and electron microscopy analyses revealed no difference in VACV gene expression or morphogenesis, the specific infectivity of VACV propagated in MEFs was lower than virus propagated in wild type (WT) cells. This lower infectivity was due to decreased VACV DNA replication during the next cycle of infection. Taken together, these results revealed that EGR-1 appears to facilitate VACV replication in starved fibroblasts by affecting viral particles infectivity.
进化使痘病毒基因组具有编码几种病毒-宿主相互作用产物的能力，这些产物干扰宿主细胞基因表达和蛋白质功能，为有效的感染创造了适当的细胞内环境。我们在这里表明，通过丝裂原活化蛋白激酶（MAPK）/ ERK（细胞外信号调节激酶）途径，牛痘病毒（VACV）在感染后 3 至 12 小时（h.p.i.）诱导小鼠胚胎成纤维细胞（MEFs）中细胞转录因子 EGR-1（早期生长反应-1）的表达。通过使用饥饿的 敲除（）MEFs，我们证明在该细胞系中，VACV 复制减少了约 1 个对数级。尽管 Western 印迹和电子显微镜分析显示 VACV 基因表达或形态发生没有差异，但在 细胞中增殖的 VACV 的特异性感染力低于在野生型（WT）细胞中增殖的病毒。这种较低的感染力是由于在下一轮感染中 VACV DNA 复制减少所致。总之，这些结果表明，EGR-1 通过影响病毒粒子感染力，似乎有助于饥饿成纤维细胞中的 VACV 复制。
