PDF(Pubmed)
Abstract：
West Nile virus (WNV) infection is a seasonal arbovirosis with the potential to cause severe neurological disease. Outcomes of the infection from WNV depend on viral factors (e.g., lineage) and host-intrinsic factors (e.g., age, sex, immunocompromising conditions). Immunity is essential to control the infection but may also prove detrimental to the host. Indeed, the persistence of high levels of pro-inflammatory cytokines and chemokines is associated with the development of blood-brain barrier (BBB) damage. Due to the importance of the inflammatory processes in the development of West Nile neuroinvasive disease (WNND), we reviewed the available literature on the subject.
According to the 2020 updated PRISMA guidelines, all peer-reviewed articles regarding the inflammatory response associated with WNND were included.
One hundred and thirty-six articles were included in the data analysis and sorted into three groups (in vitro on-cell cultures, in vivo in animals, and in humans). The main cytokines found to be increased during WNND were IL-6 and TNF-α. We highlighted the generally small quantity and heterogeneity of information about the inflammatory patterns associated with WNND.
Further studies are needed to understand the pathogenesis of WNND and to investigate the extent and the way the host inflammatory response either helps in controlling the infection or in worsening the outcomes. This might prove useful both for the development of target therapies and for the development of molecular markers allowing early identification of patients displaying an inflammatory response that puts them at a higher risk of developing neuroinvasive disease and who might thus benefit from early antiviral therapies.
According to the 2020 updated PRISMA guidelines, all peer-reviewed articles regarding the inflammatory response associated with WNND were included.
One hundred and thirty-six articles were included in the data analysis and sorted into three groups (in vitro on-cell cultures, in vivo in animals, and in humans). The main cytokines found to be increased during WNND were IL-6 and TNF-α. We highlighted the generally small quantity and heterogeneity of information about the inflammatory patterns associated with WNND.
Further studies are needed to understand the pathogenesis of WNND and to investigate the extent and the way the host inflammatory response either helps in controlling the infection or in worsening the outcomes. This might prove useful both for the development of target therapies and for the development of molecular markers allowing early identification of patients displaying an inflammatory response that puts them at a higher risk of developing neuroinvasive disease and who might thus benefit from early antiviral therapies.
摘要：
背景：西尼罗河病毒（WNV）感染是一种季节性树病，有可能导致严重的神经系统疾病。WNV感染的结果取决于病毒因子(例如，谱系)和宿主内在因素(例如，年龄,性别,免疫受损条件)。免疫对于控制感染是必不可少的，但也可能对宿主有害。的确,高水平的促炎细胞因子和趋化因子的持续存在与血脑屏障(BBB)损伤的发展相关.由于炎症过程在西尼罗河神经侵袭性疾病（WNND）发展中的重要性，我们回顾了有关该主题的现有文献。
方法：根据2020年更新的PRISMA指南，纳入了所有同行评审的有关WNND相关炎症反应的文章.
结果：数据分析中包括一百三十六篇文章，并分为三组（体外细胞培养，在动物体内，在人类中）。在WNND期间发现增加的主要细胞因子是IL-6和TNF-α。我们强调了与WNND相关的炎症模式的信息通常数量少和异质性。
结论：需要进一步的研究来了解WNND的发病机制，并研究宿主炎症反应的程度和方式有助于控制感染或恶化结局。这可能证明对于目标疗法的开发和分子标记的开发都是有用的，这些标记允许早期识别显示出炎症反应的患者，使他们处于发生神经侵袭性疾病的高风险中，因此可能从早期抗病毒疗法中受益。
方法：根据2020年更新的PRISMA指南，纳入了所有同行评审的有关WNND相关炎症反应的文章.
结果：数据分析中包括一百三十六篇文章，并分为三组（体外细胞培养，在动物体内，在人类中）。在WNND期间发现增加的主要细胞因子是IL-6和TNF-α。我们强调了与WNND相关的炎症模式的信息通常数量少和异质性。
结论：需要进一步的研究来了解WNND的发病机制，并研究宿主炎症反应的程度和方式有助于控制感染或恶化结局。这可能证明对于目标疗法的开发和分子标记的开发都是有用的，这些标记允许早期识别显示出炎症反应的患者，使他们处于发生神经侵袭性疾病的高风险中，因此可能从早期抗病毒疗法中受益。
