BACKGROUND Both vector borne and sexual transmission of Zika virus (ZIKV) involve infection of epithelial cells in the initial stages of infection. Epithelial cells are unique in their ability to form polarized monolayers and their barrier function. Cell polarity induces an asymmetry in the epithelial monolayer, which is maintained by tight junctions and specialized sorting machinery. This differential localization can have a potential impact of virus infection. Asymmetrical distribution of a viral receptor can restrict virus entry to a particular membrane while polarized sorting can lead to a directional release of virions. The present study examined the impact of cell polarity on ZIKV infection and release. METHODS A polarized Caco-2 cell model we described previously was used to assess ZIKV infection. Transepithelial resistance (TEER) was used to assess epithelial cell polarity, and virus infection was measured by immunofluorescence microscopy and qRT-PCR. Cell permeability was measured using a fluorescein leakage assay. Statistical significance was calculated using one-way ANOVA and significance was set at p < 0.05. RESULTS Using the Caco-2 cell model for polarized epithelial cells, we report that Zika virus preferentially infects polarized cells from the apical route and is released vectorially through the basolateral route. Our data also indicates that release occurs without disruption of cell permeability. CONCLUSIONS Our results show that ZIKV has directional infection and egress in a polarized cell system. This mechanism of directional infection may be one of the mechanisms that enables the cross the epithelial barrier effectively without a disruption in cell monolayer integrity. Elucidation of entry and release characteristics of Zika virus in polarized epithelial cells can lead to better understanding of virus dissemination in the host, and can help in developing effective therapeutic interventions.

中文翻译：

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Zika病毒从极化上皮细胞定向进入和释放。

背景技术寨卡病毒（ZIKV）的媒介传播和有性传播都在感染的初始阶段涉及上皮细胞的感染。上皮细胞形成极化单层的能力及其屏障功能是独特的。细胞极性在上皮单层中引起不对称，这种不对称通过紧密的连接和专门的分选机制得以维持。这种差异化的本地化可能会对病毒感染产生潜在的影响。病毒受体的不对称分布会限制病毒进入特定的膜，而极化分选会导致病毒粒子的定向释放。本研究检查了细胞极性对ZIKV感染和释放的影响。方法我们先前描述的极化Caco-2细胞模型用于评估ZIKV感染。经上皮耐药性（TEER）用于评估上皮细胞极性，并通过免疫荧光显微镜和qRT-PCR测量病毒感染。使用荧光素泄漏测定法测量细胞渗透性。使用单向方差分析计算统计学显着性，并将显着性设置为p <0.05。结果我们使用极化的上皮细胞的Caco-2细胞模型，我们报告寨卡病毒优先感染根尖途径的极化细胞，并通过基底外侧途径被矢量释放。我们的数据还表明释放发生在不破坏细胞通透性的情况下。结论我们的结果表明ZIKV在极化细胞系统中具有定向感染和外出。这种定向感染的机制可能是在不破坏细胞单层完整性的情况下有效穿越上皮屏障的机制之一。阐明寨卡病毒在极化的上皮细胞中的进入和释放特征可以使人们更好地了解宿主中的病毒传播，并有助于制定有效的治疗措施。