Suppr超能文献

猪氨基肽酶 N(CD13)受体密度对猪流行性腹泻病毒感染的贡献。

Contribution of the porcine aminopeptidase N (CD13) receptor density to porcine epidemic diarrhea virus infection.

机构信息

Department of Microbiology, College of Natural Sciences, Kyungpook National University, 1370 Sankyuk-dong, Buk-gu, Daegu 702-701, South Korea.

出版信息

Vet Microbiol. 2010 Jul 29;144(1-2):41-50. doi: 10.1016/j.vetmic.2009.12.024. Epub 2009 Dec 28.

Abstract

Porcine epidemic diarrhea virus (PEDV) and transmissible gastroenteritis virus (TGEV), which belong to group 1 coronaviruses, are important viral pathogens in pigs causing lethal diarrhea. As with the other members in the group 1, theses viruses are also known to use the host aminopeptidase N (APN) as the major receptor for cell entry. Remarkably, it was found that they utilize distinct cultured cell lines for in vitro virus propagation, since PEDV could not be replicated in swine testis (ST) cells expressing native porcine APN (pAPN), which are highly susceptible to TGEV. To explain the mechanism causing this discrimination, we postulated that there may be a correlation between the pAPN expression level and PEDV infection. As a first step toward understanding the role of cellular receptor density in PEDV replication, therefore, sub-lines of ST cells stably overexpressing recombinant pAPN were generated. We initially confirmed that the control ST cells do express relatively low levels of endogenous pAPN. In contrast, in the engineered stable cell lines, a high level of recombinant pAPN expression was demonstrated. The introduction of a pAPN gene into nonpermissive ST cells was further found to be fully sufficient to support productive infection, revealing that constitutive overexpression of pAPN can directly rescue PEDV multiplication. We further assessed whether the pAPN enzymatic function is relevant to PEDV infection. The enzymatic active motif-null mutant pAPN still retained the ability to exert its receptor activity and consequently, to cause infectious virus production. Moreover, the only APN inhibitor blocking the protease activity site had no obvious negative effect on viral infection, indicating that the enzymatic role of APN is dispensable for the process of virus replication. Taken together, our results suggest that pAPN receptor density appears to be an important factor in contributing to efficient PEDV infection.

摘要

猪流行性腹泻病毒(PEDV)和传染性胃肠炎病毒(TGEV)属于冠状病毒科 1 组,是引起猪致命性腹泻的重要病毒病原体。与 1 组的其他成员一样,这些病毒也被认为使用宿主氨肽酶 N(APN)作为细胞进入的主要受体。值得注意的是,人们发现它们使用不同的细胞系进行体外病毒繁殖,因为 PEDV 不能在表达天然猪 APN(pAPN)的猪睾丸(ST)细胞中复制,而这些细胞对 TGEV 高度敏感。为了解释导致这种差异的机制,我们假设 pAPN 的表达水平与 PEDV 感染之间可能存在相关性。因此,作为理解细胞受体密度在 PEDV 复制中的作用的第一步,我们生成了稳定过表达重组 pAPN 的 ST 细胞亚系。我们最初证实对照 ST 细胞确实表达相对较低水平的内源性 pAPN。相比之下,在工程化的稳定细胞系中,证实了高水平的重组 pAPN 表达。进一步发现,将 pAPN 基因导入非允许性 ST 细胞足以支持有活力的感染,这表明 pAPN 的组成性过表达可以直接挽救 PEDV 的增殖。我们进一步评估了 pAPN 的酶功能是否与 PEDV 感染相关。酶活性缺失突变体 pAPN 仍然保留发挥其受体活性的能力,并且仍然能够导致感染性病毒的产生。此外,唯一能阻断蛋白酶活性位点的 APN 抑制剂对病毒感染没有明显的负面影响,表明 APN 的酶功能对于病毒复制过程是可有可无的。总之,我们的结果表明,pAPN 受体密度似乎是促进 PEDV 有效感染的一个重要因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d282/7117352/093ea00f7264/gr1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验