Zika virus (ZIKV) is a flavivirus that can cause neuropathogenesis in adults and fetal neurologic malformation following the infection of pregnant women. We used a nonhuman primate model, the Indian‐origin Rhesus macaque (IRM), to gain insight into virus‐associated hallmarks of ZIKV‐induced adult neuropathology. We find that the virus causes prevalent acute and chronic neuroinflammation and chronic disruption of the blood‐brain barrier (BBB) in adult animals. ZIKV infection resulted in specific short‐ and long‐term augmented expression of the chemokine CXCL12 in the central nervous system (CNS)of adult IRMs. Moreover, CXCL12 expression persists long after the initial viral infection is apparently cleared. CXCL12 plays a key role both in regulating lymphocyte trafficking through the BBB to the CNS and in mediating repair of damaged neural tissue including remyelination. Understanding how CXCL12 expression is controlled will likely be of central importance in the definition of ZIKV‐associated neuropathology in adults.

中文翻译：

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寨卡病毒初级分离株可诱导成年猕猴的神经炎症、破坏血脑屏障并上调 CXCL12。

寨卡病毒 (ZIKV) 是一种黄病毒，可导致成人神经病变和孕妇感染后胎儿神经系统畸形。我们使用了一种非人类灵长类动物模型，即印度起源的恒河猴 (IRM)，以深入了解 ZIKV 诱导的成年神经病理学的病毒相关特征。我们发现该病毒在成年动物中引起普遍的急性和慢性神经炎症以及血脑屏障 (BBB) 的慢性破坏。ZIKV 感染导致成人 IRM 中枢神经系统 (CNS) 中趋化因子 CXCL12 的特定短期和长期增强表达。此外，CXCL12 表达在初始病毒感染明显清除后仍持续很长时间。CXCL12 在调节淋巴细胞通过 BBB 运输到 CNS 以及介导受损神经组织的修复（包括髓鞘再生）方面都起着关键作用。了解如何控制 CXCL12 表达可能对成人 ZIKV 相关神经病理学的定义至关重要。