Viruses may exploit the cardiovascular system to facilitate transmission or within-host dissemination, and the symptoms of many viral diseases stem at least in part from a loss of vascular integrity. The microvascular architecture is comprised of an endothelial cell barrier ensheathed by perivascular cells (pericytes). Pericytes are antigen-presenting cells (APCs) and play crucial roles in angiogenesis and the maintenance of microvascular integrity through complex reciprocal contact-mediated and paracrine crosstalk with endothelial cells. We here review the emerging ways that viruses interact with pericytes and pay consideration to how these interactions influence microvascular function and viral pathogenesis. Major outcomes of virus-pericyte interactions include vascular leakage or haemorrhage, organ tropism facilitated by barrier disruption, including viral penetration of the blood-brain barrier and placenta, as well as inflammatory, neurological, cognitive and developmental sequelae. The underlying pathogenic mechanisms may include direct infection of pericytes, pericyte modulation by secreted viral gene products and/or the dysregulation of paracrine signalling from or to pericytes. Viruses we cover include the herpesvirus human cytomegalovirus (HCMV, Human betaherpesvirus 5), the retrovirus human immunodeficiency virus (HIV; causative agent of acquired immunodeficiency syndrome, AIDS, and HIV-associated neurocognitive disorder, HAND), the flaviviruses dengue virus (DENV), Japanese encephalitis virus (JEV) and Zika virus (ZIKV), and the coronavirus severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2; causative agent of coronavirus disease 2019, COVID-19). We touch on promising pericyte-focussed therapies for treating the diseases caused by these important human pathogens, many of which are emerging viruses or are causing new or long-standing global pandemics.

中文翻译：

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血管周围细胞（周细胞）在病毒发病机制中的新作用

病毒可能会利用心血管系统促进传播或在宿主内传播，许多病毒性疾病的症状至少部分源于血管完整性的丧失。微血管结构由血管周围细胞（周细胞）包裹的内皮细胞屏障组成。周细胞是抗原呈递细胞 (APC)，通过与内皮细胞的复杂相互接触介导和旁分泌串扰，在血管生成和维持微血管完整性中发挥关键作用。我们在这里回顾了病毒与周细胞相互作用的新兴方式，并考虑了这些相互作用如何影响微血管功能和病毒发病机制。病毒-周细胞相互作用的主要结果包括血管渗漏或出血、屏障破坏促进的器官趋向性、包括病毒穿透血脑屏障和胎盘，以及炎症、神经、认知和发育后遗症。潜在的致病机制可能包括周细胞的直接感染、分泌的病毒基因产物对周细胞的调节和/或来自或到周细胞的旁分泌信号传导失调。我们涵盖的病毒包括疱疹病毒人类巨细胞病毒 (HCMV、人类β疱疹病毒5 )、逆转录病毒人类免疫缺陷病毒 (HIV；获得性免疫缺陷综合征、艾滋病和 HIV 相关神经认知障碍的病原体，HAND)、黄病毒登革热病毒 (DENV)、日本脑炎病毒 (JEV) 和寨卡病毒 ( ZIKV）和冠状病毒严重急性呼吸系统综合症相关冠状病毒 2（SARS-CoV-2；冠状病毒病 2019，COVID-19 的病原体）。我们谈到了有希望的以周细胞为重点的疗法，用于治疗由这些重要的人类病原体引起的疾病，其中许多是新出现的病毒或正在引起新的或长期存在的全球大流行病。