Kanangat S, Babu J S, Knipe D M, Rouse B T
Department of Microbiology, College of Veterinary Medicine, University of Tennessee, Knoxville 37996-0845, USA.
Virology. 1996 May 1;219(1):295-300. doi: 10.1006/viro.1996.0250.
Pathological effects of herpes simplex virus (HSV) can result due to a combination of direct viropathic effects and immunological reactions to viral antigens. The immunological reactions are orchestrated by a variety of cytokines and chemokines released by the host cells. Therefore, the cytokine gene expression in response to HSV-1 infection in a permissive murine cell line was investigated. The data demonstrate that HSV-1 induced a selective activation of IL-6 gene expression at the mRNA and protein levels, in the permissive cell line. The cell line used was capable of expressing IL-1, IL-7, and IL-10 in addition to IL-6, upon lipopolysaccharide stimulation. UV or heat-inactivated viruses were unable to upregulate IL-6 expression. However, mutant HSV-1 strains lacking fully functional ICP0, ICP4, ICP8, or ICP27 genes, thereby rendering them replication incompetent or impaired in in vitro cell growth (ICP0), enhanced IL-6 expression selectively. Considering the role of IL-6 in inflammation, immune response, and its known association with increased levels of MyD116 and GADD 34 mRNAs (genes involved in the prevention of apoptotic death of cells), the present data may have relevance to HSV-1-mediated diseases as well as to the prevalence of HSV-1 in the host.
单纯疱疹病毒（HSV）的病理效应可能是由直接的病毒致病作用和对病毒抗原的免疫反应共同导致的。免疫反应是由宿主细胞释放的多种细胞因子和趋化因子协调的。因此，研究了在允许性小鼠细胞系中对HSV-1感染的细胞因子基因表达。数据表明，在允许性细胞系中，HSV-1在mRNA和蛋白质水平上诱导了IL-6基因表达的选择性激活。所用细胞系在脂多糖刺激下，除了能表达IL-6外，还能表达IL-1、IL-7和IL-10。紫外线或热灭活的病毒无法上调IL-6的表达。然而，缺乏完全功能性ICP0、ICP4、ICP8或ICP27基因的突变HSV-1株，从而使其复制无能力或在体外细胞生长中受损（ICP0），却选择性地增强了IL-6的表达。考虑到IL-6在炎症、免疫反应中的作用以及其与MyD116和GADD 34 mRNA（参与防止细胞凋亡死亡的基因）水平升高的已知关联，目前的数据可能与HSV-1介导的疾病以及HSV-1在宿主体内的流行情况有关。
