Cells of human aminopeptidase N (CD13) transgenic mice are infected by human coronavirus-229E in vitro, but not in vivo
Cells of human aminopeptidase N (CD13) transgenic mice are infected by human coronavirus-229E in vitro, but not in vivo
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DOI：
10.1016/j.virol.2005.02.023
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发表时间：
2005-05-10
期刊：
影响因子：
3.7
通讯作者：
Holmes, KV
中科院分区：
文献类型：
--
作者：
Wentworth, DE;Tresnan, DB;Holmes, KV
氨肽酶 N（CD 13）是人类、猪和猫的血清学相关冠状病毒的受体。使用由 hAPN 启动子驱动的人 APN (hAPN) cDNA 创建了人冠状病毒 229E (HCoV-229E) 受体转基因小鼠系。 hAPN 转基因小鼠在肾脏、小肠、肝脏和肺中表达 hAPN mRNA。 hAPN蛋白特异性表达于近曲肾小管、支气管、肺泡囊和肠绒毛的上皮细胞上。转基因小鼠组织内的 hAPN 表达模式与小鼠 APN 的表达模式相匹配，并且在转基因杂合或纯合的小鼠中相似。来自hAPN转基因小鼠的原代胚胎细胞和骨髓树突状细胞也表达hAPN蛋白。尽管hAPN转基因小鼠在体内对HCoV-229E具有抵抗力，但在体外原代胚胎细胞和骨髓树突状细胞被感染。 hAPN 转基因小鼠作为表达 hAPN 的原代小鼠细胞的来源是有价值的。该 hAPN 转基因系还将用于与其他基因敲除、免疫缺陷或转基因小鼠的杂交实验，以鉴定除 hAPN 之外的 HCoV-229E 感染所需的因子。 (c) 2005 Elsevier Inc. 保留所有权利。
Aminopeptidase N, or CD 13, is a receptor for serologically related coronaviruses of humans, pigs, and cats. A mouse line transgenic for the receptor of human coronavirus-229E (HCoV-229E) was created using human APN (hAPN) cDNA driven by a hAPN promoter. hAPN-transgenic mice expressed hAPN mRNA in the kidney, small intestine, liver, and lung. hAPN protein was specifically expressed on epithelial cells of the proximal convoluted renal tubules, bronchi, alveolar sacs, and intestinal villi. The hAPN expression pattern within transgenic mouse tissues matched that of mouse APN and was similar in mice heterozygous or homozygous for the transgene. Primary embryonic cells and bone marrow dendritic cells derived from hAPN-transgenic mice also expressed hAPN protein. Although hAPN-transgenic mice were resistant to HCoV-229E in vivo, primary embryonic cells and bone marrow dendritic cells were infected in vitro. hAPN-transgenic mice are valuable as a source of primary mouse cells expressing hAPN. This hAPN-transgenic line will also be used for crossbreeding experiments with other knockout, immune deficient, or transgenic mice to identify factors, in addition to hAPN, that are required for HCoV-229E infection. (c) 2005 Elsevier Inc. All rights reserved.