Transfection of single‐stranded hepatitis A virus RNA activates MHC class I pathway
Transfection of single‐stranded hepatitis A virus RNA activates MHC class I pathway
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DOI：
10.1046/j.1365-2249.2002.01767.x
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发表时间：
2002-02
影响因子：
4.6
通讯作者：
Koichi Suzuki;M. Yanagi;A. Mori-Aoki;A. Mori-Aoki;Emiko Moriyama;Ken J. Ishii;L. D. Kohn;L. D. Kohn
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文献类型：
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作者：
Koichi Suzuki;M. Yanagi;A. Mori-Aoki;A. Mori-Aoki;Emiko Moriyama;Ken J. Ishii;L. D. Kohn;L. D. Kohn
尽管单链RNA病毒感染可以增强主要组织相容性复合体（MHC） I类基因的表达，但这一过程的机制尚不清楚。最近的研究表明，非免疫细胞暴露于病毒来源的双链脱氧核糖核酸（DNA）或核糖核酸（RNA）可以直接增加MHC I类和相关分子的表达，而不需要免疫细胞相互作用。在本报告中，我们发现将单链甲型肝炎病毒RNA转染到培养的肝细胞中，除了产生病毒蛋白外，还会诱导MHC I类、LMP2和抗原加工转运蛋白（TAP1）的基因。我们认为这种刺激作用是由于在单链病毒RNA复制过程中形成的双链RNA，并且涉及双链RNA依赖性蛋白激酶PKR和IFNβ的分泌。
Although infection of single‐stranded RNA viruses can enhance expression of major histocompatibility complex (MHC) class I genes, the mechanism underlying this process remains unclear. Recent studies have indicated that exposure of non‐immune cells to double‐stranded deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) of viral origin can directly increase the expression of MHC class I and related molecules without immune cell interaction. In this report, we show that transfection of single‐stranded hepatitis A virus RNA into cultured hepatocytes results in the induction of genes for MHC class I, LMP2 and transporter for antigen processing (TAP1), in addition to the generation of viral proteins. We suggest that this stimulatory effect is due to the double‐stranded RNA formed during replication of single‐stranded viral RNA, and involves both double‐stranded, RNA‐dependent protein kinase PKR and the secretion of IFNβ.