An infectious agent’s pathogenic and transmission potential is heavily influenced by early events during the asymptomatic or subclinical phase of disease. During this phase, the presence of infectious agent may be relatively low. An important example of this is Zika virus (ZIKV), which can cross the placenta and infect the foetus, even in mothers with subclinical infections. These subclinical infections represent roughly 80 % of all human infections. Initial ZIKV pathogenesis studies were performed in type I interferon receptor (IFNAR) knockout mice. Blunting the interferon response resulted in robust infectivity, and increased the utility of mice to model ZIKV infections. However, due to the removal of the interferon response, the use of these models impedes full characterization of immune responses to ZIKV-related pathologies. Moreover, IFNAR-deficient models represent severe disease whereas less is known regarding subclinical infections. Investigation of the anti-viral immune response elicited at the maternal-foetal interface is critical to fully understand mechanisms involved in foetal infection, foetal development, and disease processes recognized to occur during subclinical maternal infections. Thus, immunocompetent experimental models that recapitulate natural infections are needed. We have established subclinical intravaginal ZIKV infections in mice and guinea pigs. We found that these infections resulted in: the presence of both ZIKV RNA transcripts and infectious virus in maternal and placental tissues, establishment of foetal infections and ZIKV-mediated CXCL10 expression. These models will aid in discerning the mechanisms of subclinical ZIKV mother-to-offspring transmission, and by extension can be used to investigate other maternal infections that impact foetal development.

中文翻译：

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免疫活性豚鼠和小鼠亚临床 ZIKV 感染的特征

在疾病的无症状或亚临床阶段，传染性病原体的致病和传播潜力受到早期事件的严重影响。在这个阶段，传染性病原体的存在可能相对较低。这方面的一个重要例子是寨卡病毒 (ZIKV)，它可以穿过胎盘并感染胎儿，即使在有亚临床感染的母亲身上也是如此。这些亚临床感染约占所有人类感染的 80%。最初的 ZIKV 发病机制研究是在 I 型干扰素受体 (IFNAR) 敲除小鼠中进行的。减弱干扰素反应导致强大的感染性，并增加了小鼠模拟 ZIKV 感染的效用。然而，由于消除了干扰素反应，这些模型的使用阻碍了对 ZIKV 相关病理的免疫反应的全面表征。而且，IFNAR 缺陷模型代表严重疾病，而对亚临床感染知之甚少。研究在母胎界面引发的抗病毒免疫反应对于充分了解胎儿感染、胎儿发育和亚临床母体感染期间公认的疾病过程所涉及的机制至关重要。因此，需要能够概括自然感染的免疫活性实验模型。我们已经在小鼠和豚鼠中建立了亚临床阴道内 ZIKV 感染。我们发现这些感染导致：母体和胎盘组织中同时存在 ZIKV RNA 转录物和传染性病毒，胎儿感染的建立和 ZIKV 介导的 CXCL10 表达。