Neuroinflammation (inflammation in brain) has been known to play an important role in the development of dengue virus disease. Recently, studies from both clinical and experimental models suggest the involvement of neuroinflammation in dengue viral disease. Studies in clinical setup demonstrated that, microglial cells are actively involved in the patients having dengue virus infection, showing involvement of innate immune response in neuroinflammation. It was further proved that, clinical isolates of dengue-2 virus were able to initiate the pathologic response when injected in the mice brain. Natural killer cells were also found to play a crucial role to activate adaptive immune response. Notably, CXCL10/IFN-inducible protein 10 and CXCR3 are involved in dengue virus-mediated pathogenesis and play an important role in the development of dengue virus-mediated paralysis. In a latest report, it was seen that intracranial injection of dengue virus increases the CD8+ T-cell infiltration in brain, showing an important mechanism of neuroinflammation during the dengue virus infection. A similar study has described that, when DENV-3 is injected into the mice, it enhances the infiltration of CD8+ and CD4+ T cells as well as neutrophils. Cells immune-reactive against NS3 antigen were found throughout the brain. In conclusion, we focus on the various molecular mechanisms which contribute to the basic understanding about the role of neuroinflammation in dengue fever. These mechanisms will help in better understanding dengue pathophysiology and thus help in the development of possible therapeutics.

中文翻译：

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神经炎症与登革热病毒疾病的关系：先天和适应性免疫的重要性。

众所周知，神经炎症（脑部炎症）在登革热病毒疾病的发展中起着重要作用。最近，来自临床和实验模型的研究都表明神经炎症与登革热病毒病有关。临床研究表明，小胶质细胞积极参与登革热病毒感染的患者，显示出先天性免疫反应与神经炎症有关。进一步证明，登革2型病毒的临床分离株注射到小鼠脑中后能够启动病理反应。还发现天然杀伤细胞在激活适应性免疫应答中起关键作用。值得注意的是 CXCL10 / IFN诱导蛋白10和CXCR3参与登革热病毒介导的发病机制，并在登革热病毒介导的瘫痪发展中起重要作用。在最新报告中，可以看到颅内注射登革热病毒会增加脑中CD8 + T细胞的浸润，显示出登革热病毒感染期间神经炎症的重要机制。一项类似的研究表明，将DENV-3注射到小鼠体内后，它可以增强CD8 +和CD4 + T细胞以及嗜中性粒细胞的浸润。在整个大脑中发现了针对NS3抗原具有免疫反应性的细胞。总之，我们集中于各种分子机制，这些机制有助于对神经炎症在登革热中的作用有基本的了解。