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考克萨基病毒B感染在人类初级胰腺小岛中引发独特的细胞类型特异性反应

Daniel A Veronese-Paniagua¹, Marlie M Maestas¹, Diana C Hernandez-Rincon²

¹Roy and Diana Vagelos Division of Biology and Biomedical Sciences, Washington University School of Medicine, St. Louis, MO 63110, USA; Division of Endocrinology, Metabolism, and Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA.

|September 2, 2025

概括

人类小岛的Coxsackievirus B3 (CVB3) 感染显示出明显的细胞特异性反应,挑战了关于1型糖尿病 (T1D) 病变的病毒向的先前假设. 管道细胞,而不是β细胞,对CVB3表现出最强的免疫反应.

科学领域:

免疫学
病毒学
内分泌学

背景情况:

考克萨基病毒B (CVB) 是1型糖尿病 (T1D) 的可疑环境触发物.
对于CVB对个体岛屿细胞类型的具体影响尚不清楚.
之前的研究表明,病毒优先向β细胞和导管细胞.

研究的目的:

研究人类小岛细胞对Coxsackievirus B3 (CVB3) 感染的细胞类型特异性转录和线粒体反应.
为了澄清CVB3在人类胰腺小岛中的热带性.
确定参与小岛细胞CVB3感染的分子机制,如长非编码RNA.

主要方法:

感染CVB3的人类尸体小岛的单细胞RNA测序.
功能测试以评估病毒复制,细胞灭绝和自.
在干细胞衍生小岛中对长非编码RNAMIR7-3HG进行了降解研究.

主要成果:

在人群小岛中,CVB3感染引发了细胞类型特异的转录和线粒体反应.
没有观察到贝塔细胞或导管细胞的偏好性热带性;感染率在内分泌和外分泌区之间相似.
贝塔细胞,α细胞和管道细胞表现出最显著的转录反应,管道细胞表现出最强的干扰素和HLA反应.
发现长非编码RNA MIR7-3HG可以调节病毒RNA的表达,病毒标位,细胞亡和自.

结论:

在不同的人类小岛细胞类型中,CVB3感染会引起异质反应.
这些发现挑战了CVB3在T1D中针对特定β细胞或管道细胞的概念.
对CVB3的细胞特异性反应,包括MIR7-3HG的作用,对于理解T1D病变至关重要.

关键词:

CP:代谢过程 CP:微生物学其他:尸体胰腺小岛科克萨基病毒B 肠道病毒人类多能干细胞单细胞RNA测序转录签名一类糖尿病病毒感染

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