Cebalo L, Markotić A
Department for Virology, Croatian National Institute of Public Health, Zagreb, Croatia.
Viral Immunol. 2007 Spring;20(1):206-13. doi: 10.1089/vim.2006.0039.
Many reports suggest the hypothesis of a complex immune response accompanying hantaviral infections. However, little is known about the immunopathogenesis of nonpathogenic hantaviruses, especially Tula virus (TULV). The aim of our study was to determine the cytokine/chemokine profile induced after the infection of human macrophages with TULV and the role of viral replication in this process. Also, we wanted to establish how the study of TULV is relevant to our previous study of pathogenic hantaviruses. We showed that TULV-infected macrophages produced chemokines (interleukin-8, macrophage chemoattractant protein-1, and macrophage inflammatory protein-1beta) important for recruiting inflammatory cells, whereas no significant changes were recorded in the tested cytokine levels. This property was not influenced by ultraviolet inactivation. There were some differences in chemokine production compared with our previous study with pathogenic hantaviruses. A possible explanation could be a different way of entering host cells found in the pathogenic and nonpathogenic hantaviruses and activation of different intracellular signaling pathways.
许多报告提出了伴随汉坦病毒感染的复杂免疫反应假说。然而，对于非致病性汉坦病毒，尤其是图拉病毒（TULV）的免疫发病机制知之甚少。我们研究的目的是确定人巨噬细胞感染TULV后诱导产生的细胞因子/趋化因子谱以及病毒复制在此过程中的作用。此外，我们想确定对TULV的研究与我们之前对致病性汉坦病毒的研究有何关联。我们发现，感染TULV的巨噬细胞会产生对募集炎症细胞很重要的趋化因子（白细胞介素-8、巨噬细胞趋化蛋白-1和巨噬细胞炎症蛋白-1β），而所检测的细胞因子水平没有显著变化。这一特性不受紫外线灭活的影响。与我们之前对致病性汉坦病毒的研究相比，趋化因子的产生存在一些差异。一种可能的解释是致病性和非致病性汉坦病毒进入宿主细胞的方式不同，以及不同的细胞内信号通路被激活。
