Zika virus (ZIKV) infection has been associated with ocular abnormalities such as chorioretinal atrophy, optic nerve abnormalities, posterior uveitis and idiopathic maculopathy. Yet our knowledge about ZIKV infection in retinal cells and its potential contribution to retinal pathology is still very limited. Here we found that primary Müller cells, the principal glial cells in the retina, expressed a high level of ZIKV entry cofactor AXL gene and were highly permissive to ZIKV infection. In addition, ZIKV-infected Müller cells exhibited a pro-inflammatory phenotype and produced many inflammatory and growth factors. While a number of inflammatory signaling pathways such as ERK, p38MAPK, NF-κB, JAK/STAT3 and endoplasmic reticulum stress were activated after ZIKV infection, inhibition of p38MAPK after ZIKV infection most effectively blocked ZIKV-induced inflammatory and growth molecules. In comparison to ZIKV, Dengue virus (DENV), another Flavivirus infected Müller cells more efficiently but induced much lower pro-inflammatory responses. These data suggest that Müller cells play an important role in ZIKV-induced ocular pathology by induction of inflammatory and growth factors in which the p38MAPK pathway has a central role. Blocking p38MAPK may provide a novel approach to control ZIKV-induced ocular inflammation.

寨卡病毒（ZIKV）感染已引起眼部异常，如脉络膜视网膜萎缩，视神经异常，后葡萄膜炎和特发性黄斑病变。然而，我们对视网膜细胞中ZIKV感染及其对视网膜病理的潜在贡献的了解仍然非常有限。在这里，我们发现原发性Müller细胞（视网膜中的主要神经胶质细胞）表达高水平的ZIKV进入辅助因子AXL基因，并且高度允许ZIKV感染。此外，感染ZIKV的Müller细胞表现出促炎表型，并产生许多炎症和生长因子。虽然ZIKV感染后激活了许多炎症信号传导途径，例如ERK，p38MAPK，NF-κB，JAK / STAT3和内质网应激，ZIKV感染后p38MAPK的抑制作用最有效地阻断了ZIKV诱导的炎症和生长分子。与ZIKV登革热病毒（DENV）相比，另一种黄病毒可以更有效地感染Müller细胞，但诱导的促炎反应要低得多。这些数据表明，Müller细胞通过诱导炎症和生长因子在ZIKV诱导的眼病理中起重要作用，其中p38MAPK途径具有重要作用。阻断p38MAPK可能提供控制ZIKV诱导的眼部炎症的新方法。这些数据表明，Müller细胞通过诱导炎症和生长因子在ZIKV诱导的眼病理中起重要作用，其中p38MAPK途径具有重要作用。阻断p38MAPK可能提供控制ZIKV诱导的眼部炎症的新方法。这些数据表明，Müller细胞通过诱导炎症和生长因子在ZIKV诱导的眼病理中起重要作用，其中p38MAPK途径具有重要作用。阻断p38MAPK可能提供控制ZIKV诱导的眼部炎症的新方法。