Hirsch A J, Shenk T
Howard Hughes Medical Institute, Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA.
J Virol. 1999 Jan;73(1):404-10. doi: 10.1128/JVI.73.1.404-410.1999.
In primary human diploid fibroblasts, infection with an unpurified stock of human cytomegalovirus induced accumulation of the CC chemokine MCP-1 in the cell culture medium. By 24 h postinfection, the level of MCP-1 returned to that in uninfected cultures. When cells were infected with UV-inactivated human cytomegalovirus, the induction of MCP-1 was still observed, but no reduction was seen by 24 h postinfection or later. This effect was the result of a decrease in the level of MCP-1 mRNA present within the infected cell. Infection with purified virus revealed that the induction of MCP-1 was due to an activity found in the medium of infected cells; purified virions did not induce the expression of MCP-1. However, infection with purified virions repressed the level of MCP-1 mRNA below that found in uninfected cells. Additionally, infection with human cytomegalovirus prevented the induction of MCP-1 expression by tumor necrosis factor alpha and interleukin-1beta. The CC chemokine receptor encoded by the human cytomegalovirus US28 open reading frame (ORF) did not appear to play a role in this process, since a mutant virus in which the US28 ORF had been deleted downregulated MCP-1 in the same manner.
在原代人二倍体成纤维细胞中，用人巨细胞病毒未纯化毒株感染可诱导CC趋化因子MCP - 1在细胞培养基中积累。感染后24小时，MCP - 1水平恢复到未感染培养物中的水平。当细胞用紫外线灭活的人巨细胞病毒感染时，仍可观察到MCP - 1的诱导，但感染后24小时或之后未见下降。这种效应是由于感染细胞内MCP - 1 mRNA水平降低所致。用纯化病毒感染显示，MCP - 1的诱导是由于感染细胞培养基中发现的一种活性；纯化的病毒粒子不诱导MCP - 1的表达。然而，用纯化的病毒粒子感染会使MCP - 1 mRNA水平低于未感染细胞中的水平。此外，人巨细胞病毒感染可阻止肿瘤坏死因子α和白细胞介素 - 1β诱导MCP - 1表达。人巨细胞病毒US28开放阅读框（ORF）编码的CC趋化因子受体似乎在此过程中不起作用，因为缺失US28 ORF的突变病毒以相同方式下调MCP - 1。
