Domachowske Joseph B, Bonville Cynthia A, Easton Andrew J, Rosenberg Helene F
Department of Pediatrics, State University of New York Upstate Medical University, Syracuse, NY 13210, USA.
J Infect Dis. 2002 Jul 1;186(1):8-14. doi: 10.1086/341082. Epub 2002 Jun 14.
Pneumonia virus of mice (PVM; Paramyxoviridae, subfamily Pneumovirinae) is an important pathogen for the study of physiologically relevant acute inflammatory responses in rodent hosts. In contrast to the severe symptomatology observed in response to infection with PVM strain J3666, infection with strain 15 resulted in few clinical symptoms, limited cellular inflammatory response, and no production of macrophage inflammatory protein-1alpha or monocyte chemoattractant peptide (MCP)-1. Microarray analysis of transcripts from lung tissue indicates that PVM J3666 infection promotes up-regulation of specific proinflammatory genes, most notably interferon (IFN)-1beta, IFN response genes, and chemokines MCP-1, MCP-3, RANTES (regulated on activation, normally T cell-expressed and secreted), and eotaxin. Of these, only RANTES expression increased in response to infection with strain 15, with no increased expression of IFN or IFN response genes, despite ongoing viral replication. These results suggest that pneumovirus replication alone is insufficient to promote antiviral inflammation and that evaluation of the more divergent strain-specific pneumovirus proteins may provide some intriguing leads toward the molecular basis of this differential response.
小鼠肺炎病毒（PVM；副粘病毒科，肺炎病毒亚科）是研究啮齿动物宿主体内生理相关急性炎症反应的重要病原体。与感染PVM J3666毒株后观察到的严重症状不同，感染15毒株后临床症状很少，细胞炎症反应有限，且不产生巨噬细胞炎性蛋白-1α或单核细胞趋化蛋白（MCP）-1。对肺组织转录本的微阵列分析表明，PVM J3666感染促进了特定促炎基因的上调，最显著的是干扰素（IFN）-1β、IFN反应基因以及趋化因子MCP-1、MCP-3、调节激活正常T细胞表达和分泌因子（RANTES）和嗜酸性粒细胞趋化因子。其中，尽管病毒持续复制，但只有RANTES的表达在感染15毒株后增加，而IFN或IFN反应基因的表达没有增加。这些结果表明，仅肺炎病毒复制不足以促进抗病毒炎症反应，对差异更大的毒株特异性肺炎病毒蛋白的评估可能为这种差异反应的分子基础提供一些有趣的线索。
