Bordignon Juliano, Probst Christian M, Mosimann Ana Luiza P, Pavoni Daniela P, Stella Vanessa, Buck Gregory A, Satproedprai Nusara, Fawcett Paul, Zanata Sílvio M, de Noronha Lucia, Krieger Marco A, Duarte Dos Santos Claudia N
Instituto de Biologia Molecular do Paraná, Rua Prof Algacyr Munhoz Máder 3775, 81350-010, Curitiba, Paraná, Brazil.
Virology. 2008 Aug 1;377(2):319-29. doi: 10.1016/j.virol.2008.04.033.
Dengue virus (DENV) infection can cause a self-limiting disease (dengue fever) or a more severe clinical presentation known as dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). Furthermore, data from recent dengue epidemics in Brazil indicate that the neurological manifestations are becoming more prevalent. However, the neuropathogenesis of dengue are not well understood. The balance between viral replication efficiency and innate immunity--in opposition during the early stages of infection--determines the clinical outcome of DENV infection. In this study, we investigated the effects of DENV infection on the transcription profile of the central nervous system (CNS) of mice. We observed in infected mice the up-regulation of 151 genes possibly involved in neuropathogenesis of dengue. Conversely, they may have a protective effect. Ingenuity Systems software analysis demonstrated, that the main pathways modulated by DENV infection in the mouse CNS are involved in interferon signaling and antigen presentation.
登革病毒（DENV）感染可引发一种自限性疾病（登革热）或一种更为严重的临床表现，即登革出血热（DHF）/登革休克综合征（DSS）。此外，来自巴西近期登革热疫情的数据表明，神经学表现正变得愈发普遍。然而，登革热的神经发病机制尚未得到充分理解。病毒复制效率与先天免疫之间的平衡——在感染早期呈相反状态——决定了DENV感染的临床结果。在本研究中，我们调查了DENV感染对小鼠中枢神经系统（CNS）转录谱的影响。我们在受感染小鼠中观察到151个可能参与登革热神经发病机制的基因上调。相反，它们可能具有保护作用。Ingenuity Systems软件分析表明，DENV感染在小鼠CNS中调节的主要通路涉及干扰素信号传导和抗原呈递。
