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红细胞是 PEDV 传播的载体。

Red blood cells serve as a vehicle for PEDV transmission.

机构信息

MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu, 210095, PR China.

MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu, 210095, PR China.

出版信息

Vet Microbiol. 2021 Jun;257:109081. doi: 10.1016/j.vetmic.2021.109081. Epub 2021 Apr 20.

DOI:10.1016/j.vetmic.2021.109081
PMID:33901803
Abstract

As the most abundant cell type in the blood, red blood cells (RBCs) are serving for transporting oxygen. However, the mechanism by which RBCs binding virus remains largely unknown. Here, we demonstrated that porcine epidemic diarrhea virus (PEDV), a kind of coronavirus, could hijack RBCs and cause typical diarrhea in neonatal piglets. In an epidemiology investigation of PEDV, the RBCs samples from diarrheic pigs in several pig farms were found to be PEDV-positive. PEDV could bind to neonatal RBCs through CD71 and clathrin-mediated endocytosis, and its viability was maintained for 12 h. PEDV-loaded RBCs could transfer the virus to CD3 T cells by conjugation and reach the intestine mucosa, where it caused infection. Finally, a further animal challenge revealed that transfusing with PEDV-loaded RBCs could cause intestinal epithelial cells (IECs) infection and typical diarrhea symptom. Therefore, our studies illustrated the mechanism by which PEDV could cause intestinal infection through hijacking RBCs, further providing a novel insight into the role of RBCs as potential cells for viral transmission in coronavirus pathogenesis.

摘要

作为血液中最丰富的细胞类型,红细胞(RBC)负责运输氧气。然而,红细胞结合病毒的机制在很大程度上仍然未知。在这里,我们证明了猪流行性腹泻病毒(PEDV),一种冠状病毒,可以劫持红细胞并导致新生仔猪出现典型腹泻。在对 PEDV 的流行病学调查中,从几个猪场的腹泻猪中采集的 RBC 样本被发现呈 PEDV 阳性。PEDV 可以通过 CD71 和网格蛋白介导的内吞作用与新生 RBC 结合,其活力可维持 12 小时。载有 PEDV 的 RBC 可以通过共轭将病毒转移到 CD3 T 细胞,并到达肠黏膜,在那里引起感染。最后,进一步的动物挑战表明,输注 PEDV 负载的 RBC 可导致肠上皮细胞(IEC)感染和典型腹泻症状。因此,我们的研究阐明了 PEDV 通过劫持 RBC 引起肠道感染的机制,进一步深入了解了 RBC 作为冠状病毒发病机制中病毒传播的潜在细胞的作用。

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1
Red blood cells serve as a vehicle for PEDV transmission.红细胞是 PEDV 传播的载体。
Vet Microbiol. 2021 Jun;257:109081. doi: 10.1016/j.vetmic.2021.109081. Epub 2021 Apr 20.
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The Mechanism of PEDV-Carrying CD3 T Cells Migrate into the Intestinal Mucosa of Neonatal Piglets.PEDV 携带的 CD3 T 细胞迁移到新生仔猪肠道黏膜的机制。
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PEDV infection in neonatal piglets through the nasal cavity is mediated by subepithelial CD3 T cells.PEDV 通过鼻腔感染新生仔猪是由黏膜下 CD3 T 细胞介导的。
Vet Res. 2021 Feb 17;52(1):26. doi: 10.1186/s13567-020-00883-w.
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The enhanced replication of an S-intact PEDV during coinfection with an S1 NTD-del PEDV in piglets.在仔猪中同时感染 S1 NTD-del PEDV 时,S 完整 PEDV 的复制能力增强。
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Reduced activity of intestinal surface Na/H exchanger NHE3 is a key factor for induction of diarrhea after PEDV infection in neonatal piglets.肠道表面 Na+/H+交换器 NHE3 的活性降低是导致新生仔猪感染 PEDV 后发生腹泻的一个关键因素。
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The influence of porcine epidemic diarrhea virus on pig small intestine mucosal epithelial cell function.猪流行性腹泻病毒对猪小肠黏膜上皮细胞功能的影响。
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Deletion of a 197-Amino-Acid Region in the N-Terminal Domain of Spike Protein Attenuates Porcine Epidemic Diarrhea Virus in Piglets.删除刺突蛋白N端结构域中的一个197个氨基酸的区域可减弱仔猪猪流行性腹泻病毒的致病性。
J Virol. 2017 Jun 26;91(14). doi: 10.1128/JVI.00227-17. Print 2017 Jul 15.

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Arch Virol. 2025 May 26;170(7):139. doi: 10.1007/s00705-025-06326-1.
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Small-Molecule RAF265 as an Antiviral Therapy Acts against PEDV Infection.小分子 RAF265 作为一种抗病毒疗法,可有效对抗猪流行性腹泻病毒感染。
Viruses. 2022 Oct 15;14(10):2261. doi: 10.3390/v14102261.
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Swine coronaviruses (SCoVs) and their emerging threats to swine population, inter-species transmission, exploring the susceptibility of pigs for SARS-CoV-2 and zoonotic concerns.
猪冠状病毒 (SCoVs) 及其对猪群的新兴威胁、种间传播、探索猪对 SARS-CoV-2 的易感性和人畜共患问题。
Vet Q. 2022 Dec;42(1):125-147. doi: 10.1080/01652176.2022.2079756.
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Porcine Epidemic Diarrhea Virus Infection Disrupts the Nasal Endothelial Barrier To Favor Viral Dissemination.猪流行性腹泻病毒感染破坏鼻内皮层屏障有利于病毒传播。
J Virol. 2022 May 11;96(9):e0038022. doi: 10.1128/jvi.00380-22. Epub 2022 Apr 18.