FSTL1 and TLR4 interact with PEDV structural proteins to promote virus adsorption to host cells.

IF 4 2区 医学 Q2 VIROLOGY
Journal of Virology Pub Date : 2025-01-31 Epub Date: 2024-12-13 DOI:10.1128/jvi.01837-24
Chunyun Liu, Ning Kong, Hailong Liu, Yu Zhang, Wenzhen Qin, Wenli Zhao, Xinyu Yang, Yahe Wang, Xinyu Cao, Tian Liu, Yuchang Liu, He Sun, Wu Tong, Hai Yu, Hao Zheng, Daoliang Lan, Shengsong Xie, Guangzhi Tong, Tongling Shan
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引用次数: 0

Abstract

Infection with porcine epidemic diarrhea virus (PEDV) results in enormous economic damage to the global swine industry. PEDV starts its life cycle by binding to the receptors of host cells and adsorbing onto the cellular surfaces. However, it is still unknown how PEDV adsorbs onto the surface of host cells and the mechanism beneath the interplay of host cell transmembrane protein with PEDV proteins. FSTL1, which is a secreted glycoprotein, participates in diverse pathological and physiological processes, including immune modulation and cell proliferation and differentiation. The transmembrane protein, TLR4, serves as a pattern recognition receptor recognizing a broad spectrum of pathogens, which exerts a crucial effect on the host immune system. In this study, we identified that FSTL1 promoted PEDV infection. Further studies demonstrated the interactive relationship between FSTL1 and PEDV structural proteins (N and S2). In addition, we also confirmed that TLR4 interacted with FSTL1 and PEDV N, S1, and S2 proteins on the cell surface. Moreover, FSTL1 promoted the interaction of TLR4 and PEDV and induced viral adsorption to host cells. This study offers explicit evidence that FSTL1 and TLR4 act as mediators for host cell adsorption of PEDV by interacting with PEDV N/S proteins.IMPORTANCEAs a highly infectious porcine epidemic diarrhea virus (PEDV)-induced intestinal condition of swine, porcine epidemic diarrhea (PED) results in a 100% death rate among suckling piglets and poses a serious economic burden to global swine farming. Therefore, it is essential to investigate the mechanism of virus infection, replication, and proliferation. Virus begins its life cycle by binding to the receptor of host cells and adsorbing onto the cellular surfaces. However, it remains unclear how PEDV adsorbs onto the host cell surfaces. This study revealed that host protein FSTL1 interacted with the PEDV N and S2 proteins, while TLR4 interacted with the FSTL1 and PEDV proteins (N, S1, and S2). Moreover, we thoroughly and methodically demonstrated that FSTL1 was engaged in the PEDV internalization and attachment processes by promoting the recognition of PEDV N\S proteins by TLR4 and induced the viral adsorption to host cells.

FSTL1和TLR4与PEDV结构蛋白相互作用,促进病毒吸附到宿主细胞。
猪流行性腹泻病毒(PEDV)的感染给全球养猪业造成了巨大的经济损失。PEDV通过与宿主细胞的受体结合并吸附到细胞表面开始其生命周期。然而,PEDV如何吸附到宿主细胞表面以及宿主细胞跨膜蛋白与PEDV蛋白相互作用的机制尚不清楚。FSTL1是一种分泌糖蛋白,参与多种病理生理过程,包括免疫调节和细胞增殖分化。跨膜蛋白TLR4是一种模式识别受体,可识别多种病原体,对宿主免疫系统起着至关重要的作用。在本研究中,我们发现FSTL1促进PEDV感染。进一步的研究证实了FSTL1和PEDV结构蛋白(N和S2)之间的相互作用关系。此外,我们还证实了TLR4在细胞表面与FSTL1和PEDV N、S1和S2蛋白相互作用。FSTL1促进了TLR4与PEDV的相互作用,诱导病毒吸附到宿主细胞上。本研究提供了明确的证据,表明FSTL1和TLR4通过与PEDV N/S蛋白相互作用,作为宿主细胞吸附PEDV的介质。猪流行性腹泻(PED)是由猪流行性腹泻病毒(PEDV)引起的一种高度传染性的猪肠道疾病,在哺乳仔猪中死亡率高达100%,给全球养猪业造成了严重的经济负担。因此,研究病毒感染、复制和增殖的机制是十分必要的。病毒通过与宿主细胞的受体结合并吸附到细胞表面开始其生命周期。然而,目前尚不清楚PEDV是如何吸附到宿主细胞表面的。本研究发现宿主蛋白FSTL1与PEDV N和S2蛋白相互作用,而TLR4与FSTL1和PEDV蛋白相互作用(N、S1和S2)。此外,我们还全面而系统地证明了FSTL1通过促进TLR4对PEDV N\S蛋白的识别并诱导病毒吸附到宿主细胞上,从而参与PEDV的内化和附着过程。
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来源期刊
Journal of Virology
Journal of Virology 医学-病毒学
CiteScore
10.10
自引率
7.40%
发文量
906
审稿时长
1 months
期刊介绍: Journal of Virology (JVI) explores the nature of the viruses of animals, archaea, bacteria, fungi, plants, and protozoa. We welcome papers on virion structure and assembly, viral genome replication and regulation of gene expression, genetic diversity and evolution, virus-cell interactions, cellular responses to infection, transformation and oncogenesis, gene delivery, viral pathogenesis and immunity, and vaccines and antiviral agents.
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