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人类细胞巨型病毒pUL135蛋白通过CD2AP影响内皮细胞功能在Kawasaki疾病中

Lili Yu¹, Yucui Li², Yingying Zhang²

¹Pediatric Research Institute, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, Zhejiang, China; Key Laboratory of Structural Malformations in Childern of Zhejiang Province, 325027, Wenzhou, Zhejiang, China; Department of Pediatrics, and Key Laboratory of Children Genitourinary Diseases of Wenzhou, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

International journal of cardiology

|July 18, 2024

概括

人类细胞巨型病毒 (HCMV) 蛋白pUL135可能有助于川崎病 (KD) 的发病. 在KD小鼠模型中,发现这种病毒蛋白会损害内皮细胞功能,并恶化冠状动脉炎,这表明它在KD血管损伤中发挥了作用.

科学领域:

病毒学病毒学
免疫学免疫学免疫学
儿童心脏病学儿童心脏病学

背景情况:

川崎病 (KD) 是一种小儿血管炎,原因不明,可能是传染性的.
人类细胞巨乳病毒 (HCMV) 感染各种细胞,其蛋白质pUL135对于病毒活性和免疫逃避至关重要.

研究的目的:

研究HCMV蛋白pUL135在Kawasaki疾病病原发生中的潜在作用.
在KD模型中检查pUL135对内皮细胞和心脏炎症的影响.

主要方法:

在KD患者血清中量化pUL135水平.
评估了pUL135对内皮细胞增殖,迁移和actin细胞骨架的影响.
在小鼠KD模型中评估pUL135对心脏炎症的影响.

主要成果:

在KD患者的血清中,pUL135水平升高.
pUL135抑制了内皮细胞的增殖,迁移和管形成,影响了actin细胞骨架.
在KD小鼠模型中,pUL135表达加剧了冠状动脉炎,通过CD2AP进行介导.

结论:

HCMV pUL135 导致内皮功能障碍.
pUL135在卡瓦萨基病中加剧冠状动脉损伤方面发挥作用.

关键词:

CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP CD2AP 内皮质功能障碍内皮质功能障碍这就是HCMV.川崎病是川崎病的一种疾病.在pUL1355中,

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