The effect of rhinovirus on airway epithelium is very well described. However, its influence on the vascular endothelium is unknown. The current study assesses the effect of rhinovirus HRV16 on the antiviral and inflammatory response in the human vascular endothelial cells (ECs). HRV16 increased IFN‐β, RANTES, and IP‐10 mRNA expression and protein release. HRV16 copy number in ECs reached maximal value 10 h after incubation. Increase in virus copies was accompanied by the enhancement of Toll‐ and RIG‐I‐like receptors: TLR3, RIG‐I, and MDA5. Additionally, HRV16 increased OAS‐1 and PKR mRNA expression, enzymes responsible for virus degradation and inhibition of replication. ICAM‐1 blockade decreased HRV16 copy number in ECs and inhibited IFN‐β, RANTES, IP‐10, OAS1, PKR, TLR3, RIG‐I, and MDA5 mRNA expression increase upon subsequent induction with HRV16. The vascular endothelium may be infected by human rhinovirus and generate antiviral and inflammatory innate response. Results of the study indicate the possible involvement of the vascular endothelium in the immunopathology of rhinoviral airway infections.

中文翻译：

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人鼻病毒16在人血管内皮中诱导抗病毒和炎症反应


鼻病毒对气道上皮的影响已有很好的描述。然而，其对血管内皮的影响尚不清楚。目前的研究评估了鼻病毒 HRV16 对人类血管内皮细胞 (EC) 抗病毒和炎症反应的影响。 HRV16 增加 IFN-β、RANTES 和 IP-10 mRNA 表达和蛋白质释放。 ECs中的HRV16拷贝数在孵育10小时后达到最大值。病毒拷贝数的增加伴随着 Toll 和 RIG-I 样受体的增强：TLR3、RIG-I 和 MDA5。此外，HRV16 增加了 OAS-1 和 PKR mRNA 的表达，这些酶负责病毒降解和抑制复制。 ICAM-1 阻断可减少 EC 中的 HRV16 拷贝数，并抑制随后用 HRV16 诱导后的 IFN-β、RANTES、IP-10、OAS1、PKR、TLR3、RIG-I 和 MDA5 mRNA 表达增加。血管内皮可能被人鼻病毒感染并产生抗病毒和炎症先天反应。研究结果表明血管内皮可能参与鼻病毒气道感染的免疫病理学。