Department of Microbiology and Molecular Medicine, University of Geneva, Geneva, Switzerland.
Bioinformatics Support Platform, University of Geneva, Geneva, Switzerland.
PLoS Pathog. 2022 Jul 5;18(7):e1010632. doi: 10.1371/journal.ppat.1010632. eCollection 2022 Jul.
Enteroviruses (EVs) are among the most prevalent viruses worldwide. They are characterized by a high genetic and phenotypic diversity, being able to cause a plethora of symptoms. EV-D68, a respiratory EV, and EV-D94, an enteric EV, represent an interesting paradigm of EV tropism heterogeneity. They belong to the same species, but display distinct phenotypic characteristics and in vivo tropism. Here, we used these two viruses as well as relevant 3D respiratory, intestinal and neural tissue culture models, to highlight key distinctive features of enteric and respiratory EVs. We emphasize the critical role of temperature in restricting EV-D68 tissue tropism. Using transcriptomic analysis, we underscore fundamental differences between intestinal and respiratory tissues, both in the steady-state and in response to infection. Intestinal tissues present higher cell proliferation rate and are more immunotolerant than respiratory tissues. Importantly, we highlight the different strategies applied by EV-D94 and EV-D68 towards the host antiviral response of intestinal and respiratory tissues. EV-D68 strongly activates antiviral pathways while EV-D94, on the contrary, barely induces any host defense mechanisms. In summary, our study provides an insightful characterization of the differential pathogenesis of EV-D68 and EV-D94 and the interplay with their main target tissues.
肠道病毒(EVs)是世界范围内最常见的病毒之一。它们具有高度的遗传和表型多样性,能够引起多种症状。肠道病毒 D68(EV-D68)和肠道病毒 D94(EV-D94)是呼吸道肠道病毒,它们代表了肠道病毒嗜性异质性的有趣范例。它们属于同一物种,但表现出不同的表型特征和体内嗜性。在这里,我们使用这两种病毒以及相关的 3D 呼吸道、肠道和神经组织培养模型,突出肠道和呼吸道 EV 的关键区别特征。我们强调温度在限制 EV-D68 组织嗜性方面的关键作用。通过转录组分析,我们强调了在稳态和感染反应中肠道和呼吸道组织之间的根本差异。肠道组织的细胞增殖率较高,比呼吸道组织具有更高的免疫耐受性。重要的是,我们强调了 EV-D94 和 EV-D68 针对肠道和呼吸道组织的宿主抗病毒反应所采用的不同策略。EV-D68 强烈激活抗病毒途径,而 EV-D94 则几乎不诱导任何宿主防御机制。总之,我们的研究提供了对 EV-D68 和 EV-D94 的差异发病机制及其与主要靶组织相互作用的深入了解。