Preclinical Evaluation of a Phage T4‐Based Multi‐Epitope Nanoparticle Vaccine Against Porcine Epidemic Diarrhea Virus

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作者 GuoQing Zhao; ShiDan Zhang; YuMin Zhang; ShengJing Jiao; XiaoYan Zeng; LuRu Zhao; Jie Wang; JingJiao Ma; YuQiang Cheng; HengAn Wang; YaXian Yan; JianHe Sun; ZhaoFei Wang 期刊 Transboundary and Emerging Diseases 发表日期 2026 卷/期/页码 Vol. 2026(1) ISSN 1865-1674 DOI 10.1155/tbed/8438783 类型 原创研究 (Original Research)

📄 英文摘要 English Abstract

EN

Porcine epidemic diarrhea virus (PEDV) continues to threaten the global swine industry, and currently available vaccines often provide incomplete protection against emerging virulent strains. In this study, we developed a phage T4‐based multi‐epitope nanoparticle vaccine targeting PEDV. B and T cell epitopes derived from the PEDV spike (S) protein were identified through immunoinformatic analyses and assembled into a tandem epitope construct (Pep) using flexible linkers. In silico analyses predicted favorable antigenic properties of Pep and a stable interaction with Toll‐like receptor 3 (TLR3). The recombinant Pep protein was expressed in

Escherichia coli and subsequently displayed on T4 phage to generate the T4‐Pep vaccine. Characterization revealed that each phage carried approximately 800 copies of Pep. In mice, immunization with T4‐Pep induced significantly higher PEDV‐specific IgG levels and virus‐neutralizing antibody titers than immunization with the Pep. Following PEDV challenge, T4‐Pep–immunized mice showed improved protection and reduced intestinal damage, as confirmed by histopathological analysis. Together, these findings highlight the potential of phage T4 as an efficient and immunogenic platform for delivering viral epitopes, offering a promising strategy for the development of vaccines against PEDV and related pathogens.

📄 中文摘要 Chinese Abstract

中文
猪流行性腹泻病毒(PEDV)主要通过粪-口途径传播,并主要感染动物肠道。哺乳仔猪对PEDV感染尤为易感,死亡率可达50%至100%。该病毒对肠上皮细胞具有显著趋向性,可诱导严重绒毛萎缩,最终导致吸收不良性腹泻、脱水乃至死亡。尽管传统疫苗可用于预防PEDV,但其在应对新出现的变异毒株时效果并不理想。 基于表位的疫苗已成为一类有前景的免疫原,尤其在兽医学领域。PEDV的刺突(S)蛋白是中和抗体的主要靶标,包含多种对保护性免疫至关重要的免疫显性B细胞和T细胞表位。然而,仅肽基抗原通常免疫原性较差,需要高效的递送系统或免疫刺激佐剂才能诱发充分免疫应答。T4噬菌体已成为一种多功能且免疫原性强的疫苗平台,其重复衣壳结构可激活模式识别受体,并通过多价抗原呈递强烈激活B细胞受体。

📋 英文结构化总结 English Structured Summary

全文整理

EN

Background:

Porcine epidemic diarrhea virus (PEDV) is chiefly transmitted via the fecal‐oral route and primarily infects the animal’s intestines. Suckling piglets are especially vulnerable to PEDV infection, with mortality rates ranging from 50% to 100%. The virus exhibits a marked tropism for intestinal epithelial cells, inducing severe villous atrophy that culminates in malabsorptive diarrhea, dehydration, and ultimately, death. Although conventional vaccines are used to prevent PEDV, they are not very effective against emerging variant strains.

Epitope‐based vaccines have emerged as a promising class of immunogens, particularly within veterinary medicine. The spike (S) protein of PEDV represents the primary target for neutralizing antibodies and encompasses multiple immunodominant B‐ and T‐cell epitopes essential for protective immunity. However, peptide‐based antigens alone are typically poorly immunogenic and necessitate efficient delivery systems or immunostimulatory adjuvants to provoke adequate responses. The T4 bacteriophage has emerged as a versatile and highly immunogenic vaccine platform, with repetitive capsid architecture that can activate pattern recognition receptors and strongly activate B‐cell receptors through multivalent antigen presentation.

Methods:

The PEDV S protein (GenBank: AVK78141.1) was used for epitope prediction. B‐cell epitopes were identified using ABCpred with 16 residues and a threshold of 0.85, yielding 29 candidate epitopes, and using ElliPro with a minimum score of 0.5 and a maximum distance of 6 Å, yielding 28 candidate epitopes. Overlapping sequences were integrated, and candidates were filtered using VaxiJen for antigenicity and ToxinPred2 for toxicity. Helper T‐cell epitopes were predicted with NetMHCpanII‐4.1 for H2‐IAb with length 15 and VaxiJen score exceeding 0.4. Cytotoxic T‐lymphocyte epitopes were predicted with NetMHCpan‐4.1 for multiple SLA class I alleles with length nine and VaxiJen score above 1.2.

Selected epitopes were concatenated using AAY, EAAAK, KK, and GPGPG linkers, and the CDCRGDCFC peptide was conjugated via an EAAAK linker to form the construct Pep. The three‐dimensional structure of Pep was predicted using AlphaFold2, epitopes were mapped onto the S protein structure (PDB ID: 6U7K) using ChimeraX, and molecular docking with Toll‐like receptor 3 (TLR3) was performed using ClusPro. Immunogenicity was simulated using C‐ImmSim, and molecular dynamics simulations were performed using iMODS. The Pep gene was cloned into pET‐28a and pRbSoc plasmids, expressed in Escherichia coli, and purified. Soc‐Pep was conjugated to T4 Soc− phage at molar ratios from 1:1 to 32:1 to generate the T4‐Pep vaccine, and Pep copy number per phage was calculated.

Female BALB/C mice were divided into four groups (n = 9 each): PBS, T4, T4‐Pep, and Pep. Mice received oral vaccinations at weeks 0, 2, 4, and 6, with the T4‐Pep group receiving 1.2 × 10^12 PFU T4‐Pep phage, equivalent to 50 μg of Pep. Serum was collected 14 days after each immunization. On day 15 after the third boost, mice were orally inoculated with 100 TCID 50 of PEDV‐CHN/SH‐2012‐5/2012. Body weight was recorded daily, and proximal jejunal tissues were collected at 7 days post‐challenge for hematoxylin and eosin staining and qRT‐PCR. PEDV‐specific IgG was measured by ELISA, and neutralizing antibodies were determined by a virus neutralization assay. Statistical analysis was performed using GraphPad Prism 8.0.2.

Results:

Transmembrane‐topology analysis showed that amino acids 19–1326 of the PEDV S protein lack transmembrane segments and are suitable for epitope screening. The selected epitopes were nontoxic and were mostly located within the S1 region. Sequence alignment of S proteins from various PEDV strains, including the highly pathogenic G2c strain, revealed over 91% similarity, with the identified linear epitopes being highly conserved. Molecular docking showed that Pep formed stable interactions with TLR3, with key hydrogen bonds involving Pep residues Glu38, Tyr36, Glu35, Ser31, and Arg33. iMODS analysis indicated a stable Pep‐TLR3 complex, and C‐ImmSim predicted that Pep activated B cells, natural killer cells, macrophages, and T cells, with high IgG antibody levels and consistently high cytokine concentrations.

The Soc‐Pep fusion protein was expressed and purified, and Pep alone failed to bind T4 Soc−, confirming Soc‐dependent binding. Display levels increased with the input ratio and reached saturation at approximately 16:1. The average Pep copy number was approximately 850 copies per phage, and Western blotting confirmed that T4‐Pep was specifically recognized by PEDV‐positive mouse serum. In mice, immunization with T4‐Pep induced significantly higher PEDV‐specific IgG levels and virus‐neutralizing antibody titers than immunization with Pep alone.

Following PEDV challenge, T4‐Pep–immunized mice maintained relatively stable body weights, whereas T4 and PBS groups exhibited progressive weight loss. Histopathological analysis showed that T4‐Pep–immunized mice had intact small intestinal villi with no significant pathological alterations, while T4 and PBS groups showed marked villus atrophy and damage, and the Pep group showed mild villus injury and crypt hyperplasia. Viral load in intestinal tissues was significantly lower in T4‐Pep–vaccinated mice than in Pep–vaccinated mice.

Data Summary:

Epitope prediction generated 29 ABCpred candidates and 28 ElliPro candidates. The final selected epitopes included BCL1 (antigenicity 0.5620), BCL2 (0.9787), BCL3 (0.5069), BCL4 (0.6834), CTL1 (1.5570), CTL2 (1.3770), HTL1 (0.4039), and HTL2 (0.4278), all predicted as nontoxic. Sequence conservation analysis reported over 91% similarity among analyzed PEDV strains, and the Discussion reported over 91.46% similarity. The Pep‐TLR3 complex had a calculated eigenvalue of 2.234809 × 10^−6, and most deformability peaks were below 0.5. The abstract reported approximately 800 copies of Pep per phage, while the characterization section reported an average of approximately 850 copies per phage.

Mouse experiments used four groups with n = 9 per group. The T4‐Pep dose was 1.2 × 10^12 PFU, equivalent to 50 μg of Pep, and challenge used 100 TCID 50 of PEDV. T4‐Pep immunization induced a peak PEDV‐specific IgG titer of 5 × 10^4 and higher neutralizing antibody titers than Pep alone. Antibody and viral load analyses were reported with n = 3, while body weight and villus length measurements were reported with n = 6. T4‐Pep–immunized mice showed reduced intestinal damage and significantly lower jejunal viral load than Pep–immunized mice.

Conclusions:

The T4‐Pep multi‐epitope nanoparticle vaccine induced significantly stronger PEDV‐specific IgG and neutralizing antibody responses than free Pep and provided improved protection against PEDV challenge in mice. The T4 phage platform enhanced the immunogenicity of the multi‐epitope construct, reduced intestinal damage, and lowered viral load, supporting its potential as an efficient and immunogenic platform for delivering viral epitopes.

The conserved epitopes derived from the PEDV S protein may support cross‐protection against multiple PEDV variants, including emerging strains. The authors noted that further validation in porcine models, direct mucosal immune measurements, and clarification of the protective mechanisms of epitope‐based immunization are required.

Practical Significance:

This study provides a practical phage T4–based strategy for developing PEDV vaccines that may better address incomplete protection against emerging virulent strains. The oral T4‐Pep nanoparticle platform offers a feasible approach for veterinary vaccine development against PEDV and related pathogens by improving antigen presentation and immune activation.

📋 中文结构化总结 Chinese Structured Summary

中文

背景:

猪流行性腹泻病毒(PEDV)主要通过粪-口途径传播,并主要感染动物肠道。哺乳仔猪对PEDV感染尤为易感,死亡率可达50%至100%。该病毒对肠上皮细胞具有显著趋向性,可诱导严重绒毛萎缩,最终导致吸收不良性腹泻、脱水乃至死亡。尽管传统疫苗可用于预防PEDV,但其在应对新出现的变异毒株时效果并不理想。

基于表位的疫苗已成为一类有前景的免疫原,尤其在兽医学领域。PEDV的刺突(S)蛋白是中和抗体的主要靶标,包含多种对保护性免疫至关重要的免疫显性B细胞和T细胞表位。然而,仅肽基抗原通常免疫原性较差,需要高效的递送系统或免疫刺激佐剂才能诱发充分免疫应答。T4噬菌体已成为一种多功能且免疫原性强的疫苗平台,其重复衣壳结构可激活模式识别受体,并通过多价抗原呈递强烈激活B细胞受体。

方法:

采用PEDV S蛋白(GenBank:AVK78141.1)进行表位预测。B细胞表位使用ABCpred进行预测,窗口为16个残基,阈值为0.85,获得29个候选表位;使用ElliPro进行预测,最低得分为0.5,最大距离为6 Å,获得28个候选表位。对重叠序列进行合并,并使用VaxiJen对抗原性、ToxinPred2对毒性进行筛选。辅助性T细胞表位采用NetMHCpanII-4.1针对H2-IAb、长度为15且VaxiJen得分大于0.4进行预测。细胞毒性T淋巴细胞表位采用NetMHCpan-4.1针对多个SLA I类等位基因、长度为9且VaxiJen得分高于1.2进行预测。

将所选表位使用AAY、EAAAK、KK和GPGPG连接肽串联,并通过EAAAK连接肽偶联CDCRGDCFC肽,构建Pep。使用AlphaFold2预测Pep的三维结构,使用ChimeraX将表位映射至S蛋白结构(PDB ID:6U7K),并使用ClusPro进行与Toll样受体3(TLR3)的分子对接。使用C-ImmSim模拟免疫原性,并使用iMODS进行分子动力学模拟。将Pep基因克隆至pET-28a和pRbSoc质粒中,在大肠杆菌中表达并纯化。将Soc-Pep以1:1至32:1的摩尔比偶联至T4 Soc−噬菌体,制备T4-Pep疫苗,并计算每个噬菌体的Pep拷贝数。

将雌性BALB/C小鼠分为4组(每组n = 9):PBS组、T4组、T4-Pep组和Pep组。小鼠于第0、2、4和6周经口免疫,T4-Pep组给予1.2 × 10^12 PFU T4-Pep噬菌体,相当于50 μg Pep。每次免疫后14天采集血清。第三次加强免疫后第15天,小鼠经口攻毒,攻毒剂量为100 TCID50的PEDV-CHN/SH-2012-5/2012。每日记录体重,攻毒后7天采集空肠近端组织,进行苏木精-伊红染色和qRT-PCR检测。采用ELISA检测PEDV特异性IgG,采用病毒中和试验检测中和抗体。使用GraphPad Prism 8.0.2进行统计分析。

结果:

跨膜拓扑分析显示,PEDV S蛋白第19–1326位氨基酸不含跨膜区段,适合进行表位筛选。所选表位均无毒性,且主要位于S1区域。对多种PEDV毒株(包括高致病性G2c毒株)S蛋白进行序列比对,显示相似度超过91%,所鉴定的线性表位高度保守。分子对接显示,Pep与TLR3形成稳定相互作用,关键氢键涉及Pep残基Glu38、Tyr36、Glu35、Ser31和Arg33。iMODS分析表明Pep-TLR3复合物稳定,C-ImmSim预测Pep可激活B细胞、自然杀伤细胞、巨噬细胞和T细胞,并产生高水平IgG抗体和持续高浓度细胞因子。

Soc-Pep融合蛋白成功表达并纯化,单独Pep不能结合T4 Soc−,证实结合依赖于Soc。展示水平随加入比例增加而升高,并在约16:1时达到饱和。平均Pep拷贝数约为每个噬菌体850拷贝,Western blot证实T4-Pep可被PEDV阳性小鼠血清特异性识别。在小鼠中,T4-Pep免疫诱导的PEDV特异性IgG水平和病毒中和抗体滴度显著高于单独Pep免疫。

PEDV攻毒后,T4-Pep免疫小鼠体重保持相对稳定,而T4组和PBS组出现进行性体重下降。组织病理学分析显示,T4-Pep免疫小鼠小肠绒毛完整,未见明显病理改变;T4组和PBS组出现明显绒毛萎缩和损伤;Pep组出现轻度绒毛损伤和隐窝增生。T4-Pep免疫小鼠肠道组织中的病毒载量显著低于Pep免疫小鼠。

数据摘要:

表位预测共获得29个ABCpred候选表位和28个ElliPro候选表位。最终选定的表位包括BCL1(抗原性0.5620)、BCL2(0.9787)、BCL3(0.5069)、BCL4(0.6834)、CTL1(1.5570)、CTL2(1.3770)、HTL1(0.4039)和HTL2(0.4278),均预测为无毒性。序列保守性分析显示,所分析的PEDV毒株间相似度超过91%,讨论部分报告相似度超过91.46%。Pep-TLR3复合物的计算特征值为2.234809 × 10^−6,大多数变形性峰值低于0.5。摘要报告每个噬菌体约800拷贝Pep,而表征部分报告平均约850拷贝/噬菌体。

小鼠实验采用4组,每组n = 9。T4-Pep剂量为1.2 × 10^12 PFU,相当于50 μg Pep,攻毒使用100 TCID50 PEDV。T4-Pep免疫诱导的PEDV特异性IgG峰值滴度为5 × 10^4,且中和抗体滴度高于单独Pep免疫。抗体和病毒载量分析以n = 3报告,体重和绒毛长度测量以n = 6报告。T4-Pep免疫小鼠肠道损伤减轻,空肠病毒载量显著低于Pep免疫小鼠。

结论:

T4-Pep多表位纳米颗粒疫苗诱导的PEDV特异性IgG和中和抗体应答显著强于游离Pep,并在小鼠中提供了对PEDV攻毒的更好保护。T4噬菌体平台增强了多表位构建体的免疫原性,减轻了肠道损伤并降低了病毒载量,支持其作为递送病毒表位的高效且免疫原性强的平台的潜力。

来源于PEDV S蛋白的保守表位可能支持对多种PEDV变异毒株(包括新出现毒株)的交叉保护。作者指出,仍需在小鼠模型以外的猪模型中进一步验证,直接检测黏膜免疫指标,并阐明基于表位免疫的保护机制。

实际意义:

本研究提供了一种实用的基于T4噬菌体的PEDV疫苗开发策略,可能更好地应对新出现强毒株保护不完全的问题。口服T4-Pep纳米颗粒平台通过改善抗原呈递和免疫激活,为PEDV及相关病原体的兽用疫苗开发提供了可行途径。

📖 英文全文 English Full Text

EN

pmc Transbound Emerg Dis Transbound Emerg Dis 4732 tbed TBED Transboundary and Emerging Diseases 1865-1674 1865-1682 Wiley PMC13266086 PMC13266086.1 13266086 13266086 42290005 10.1155/tbed/8438783 TBED8438783 1 Research Article Article Preclinical Evaluation of a Phage T4‐Based Multi‐Epitope Nanoparticle Vaccine Against Porcine Epidemic Diarrhea Virus Zhao GuoQing https://orcid.org/0009-0009-5011-5942

1 Zhang ShiDan 1 Zhang YuMin 1 Jiao ShengJing 1 Zeng XiaoYan

1 Zhao LuRu 1 Wang Jie 1 Ma JingJiao 1 Cheng YuQiang

1 Wang HengAn 1 Yan YaXian 1 Sun JianHe https://orcid.org/0000-0002-4005-6071

1 sunjhe@sjtu.edu.cn Wang ZhaoFei https://orcid.org/0000-0002-4524-9657

1 wzfxlzjx@sjtu.edu.cn Chen Nan-hua chnhlh@126.com

1

Shanghai Key Laboratory of Veterinary Biotechnology , School of Agriculture and Biology , Shanghai Jiao Tong University , Shanghai , 201100 , China , sjtu.edu.cn

14 6 2026 2026 2026 503610 8438783 19 5 2026 11 3 2026

21 5 2026 14 06 2026 16 06 2026 17 06 2026 Copyright © 2026 GuoQing Zhao et al. Transboundary and Emerging Diseases published by John Wiley & Sons Ltd. 2026 https://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the https://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. Porcine epidemic diarrhea virus (PEDV) continues to threaten the global swine industry, and currently available vaccines often provide incomplete protection against emerging virulent strains. In this study, we developed a phage T4‐based multi‐epitope nanoparticle vaccine targeting PEDV. B and T cell epitopes derived from the PEDV spike (S) protein were identified through immunoinformatic analyses and assembled into a tandem epitope construct (Pep) using flexible linkers. In silico analyses predicted favorable antigenic properties of Pep and a stable interaction with Toll‐like receptor 3 (TLR3). The recombinant Pep protein was expressed in Escherichia coli and subsequently displayed on T4 phage to generate the T4‐Pep vaccine. Characterization revealed that each phage carried approximately 800 copies of Pep. In mice, immunization with T4‐Pep induced significantly higher PEDV‐specific IgG levels and virus‐neutralizing antibody titers than immunization with the Pep. Following PEDV challenge, T4‐Pep–immunized mice showed improved protection and reduced intestinal damage, as confirmed by histopathological analysis. Together, these findings highlight the potential of phage T4 as an efficient and immunogenic platform for delivering viral epitopes, offering a promising strategy for the development of vaccines against PEDV and related pathogens. Keywords epitopes phage porcine epidemic diarrhea virus vaccine

Science and Technology Commission of Shanghai Municipality 10.13039/501100003399

23N51900300 National Natural Science Foundation of China 10.13039/501100001809

32373097 pmc-status-qastatus 0 pmc-status-live yes pmc-status-embargo no pmc-status-released yes pmc-prop-open-access yes pmc-prop-olf no pmc-prop-manuscript no pmc-prop-legally-suppressed no pmc-prop-has-pdf yes pmc-prop-has-supplement no pmc-prop-pdf-only no pmc-prop-suppress-copyright no pmc-prop-is-real-version no pmc-prop-is-scanned-article no pmc-prop-preprint no pmc-prop-in-epmc yes pmc-license-ref CC BY source-schema-version-number 2.0 cover-date 2026 details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.8.0 mode:remove_FC converted:15.06.2026

Zhao , GuoQing ,

Zhang , ShiDan ,

Zhang , YuMin ,

Jiao , ShengJing ,

Zeng , XiaoYan ,

Zhao , LuRu ,

Wang , Jie ,

Ma , JingJiao ,

Cheng , YuQiang ,

Wang , HengAn ,

Yan , YaXian ,

Sun , JianHe ,

Wang , ZhaoFei , Preclinical Evaluation of a Phage T4‐Based Multi‐Epitope Nanoparticle Vaccine Against Porcine Epidemic Diarrhea Virus ,

Transboundary and Emerging Diseases , 2026 , 8438783 , 13 pages, 2026 .

10.1155/tbed/8438783 42290005 GuoQing Zhao and ShiDan Zhang contributed equally to this work.

Academic Editor: Nan‐hua Chen 1. Introduction Porcine epidemic diarrhea virus (PEDV) is chiefly transmitted via the fecal‐oral route and primarily infects the animal’s intestines [ 1 ]. Suckling piglets are especially vulnerable to PEDV infection. Following infection, mortality rates range from 50% to 100% [ 2 , 3 ]. The virus exhibits a marked tropism for intestinal epithelial cells, inducing severe villous atrophy that culminates in malabsorptive diarrhea, dehydration, and ultimately, death [ 4 ]. Although conventional vaccines are used to prevent PEDV, they are not very effective against emerging variant strains [ 5 , 6 ]. Following vaccination, cells trigger a complex series of immune responses [ 7 ]. Virus‐infected cells are primarily eliminated through Cytotoxic T lymphocytes (CTL)‐mediated immune responses [ 8 ]. Concurrently, helper T‐cell epitopes (HTL) facilitate B cell activation and differentiation, leading to the production of antibodies [ 9 ]. Employing immunoinformatic tools to predict epitopes for B and T lymphocytes has significantly speeded up the design and development of antiviral vaccines. Currently, research into vaccines for PEDV encompasses a variety of technical approaches. These include live‐attenuated and inactivated PEDV vaccines [ 10 ]; an oral PEDV vaccine based on cationic liposomes [ 11 ]; a subunit vaccine [ 12 ]; nanoparticle vaccines [ 13 ]; and mRNA PEDV vaccines encapsulated in lipid nanoparticles [ 14 ], to name a few. However, PEDV has evolved and mutated due to external pressures, making it increasingly difficult to prevent and control [ 6 , 15 ]. The PEDV virus is still tricky to contain successfully [ 16 , 17 ]. Currently, epitope‐based vaccines have emerged as a promising class of immunogens, particularly within veterinary medicine [ 5 ]. Subunit vaccines incorporating defined viral epitopes offer a compelling alternative to traditional approaches, combining enhanced safety profiles with the capacity for precise immune targeting. The spike (S) protein of PEDV, which facilitates viral attachment and membrane fusion, represents the primary target for neutralizing antibodies and encompasses multiple immunodominant B‐ and T‐cell epitopes essential for protective immunity [ 18 , 19 ]. However, peptide‐based antigens alone are typically poorly immunogenic and necessitate efficient delivery systems or immunostimulatory adjuvants to provoke adequate responses. The T4 bacteriophage has recently been used to develop vaccines by displaying antigens on its capsid surface [ 20 , 21 ]. T4 bacteriophage has emerged as a versatile and highly immunogenic vaccine platform. Its surface architecture features two dispensable capsid proteins—Soc and Hoc—which permit the display of heterologous peptides through either genetic fusion or chemical conjugation [ 22 ]. Studies have shown that the T4 phage vector can enhance the immune response independently [ 23 ]. Furthermore, the repetitive and symmetrical arrangement of T4 phage capsid proteins resembles the pathogen‐associated molecular patterns (PAMPs) of human viruses that activate pattern recognition receptors (PRRs). These features likely bind to extracellular PRRs, triggering the transmission of inflammatory signals [ 24 ]. Additionally, the large quantity of the major T4 phage capsid protein enables antigens to be incorporated into the phage in a concentrated manner. This multivalent presentation strongly activates B‐cell receptors, thereby inducing a robust humoral immune response. This property may also optimize immunogenicity by regulating the antigen copy number and spacing [ 25 ]. By leveraging the innate immunostimulatory properties of bacteriophages, phage‐based vaccine platforms circumvent many limitations associated with conventional vaccine approaches, enhancing the immunogenicity of target antigens [ 22 , 26 ]. In addition, phages themselves can induce immune responses [ 27 ]. Recent progress in phage‐based delivery systems has opened new avenues for commercial vaccine development [ 28 ]. Collectively, these advances support the exploration of novel phage‐vectored vaccines against PEDV as a promising strategy to mitigate outbreaks. There is accumulating evidence that the T4 bacteriophage has great potential as a vaccine platform against viruses [ 21 , 26 ]. This research utilized bioinformatics to identify epitopes within the S protein of PEDV. These epitopes were then assembled in tandem and displayed on T4 phages using an in vitro assembly method. Subsequent evaluation of their properties and immunogenicity suggests that this construct holds promise as a vaccine candidate, providing both a theoretical and practical basis for PEDV prevention and control. 2. Materials and Methods 2.1. Prediction of Epitopes The PEDV S protein (GenBank: AVK78141.1 ) served as the template for epitope prediction. In parallel, we obtained the S protein sequences of various PEDV genotypes from the NCBI database and performed an alignment analysis using ESPript 3.2 [ 29 ]. The ABCpred [ 30 ] was employed to identify B‐cell epitopes (BCL) of 16 residues and a threshold of 0.85, yielding 29 candidate epitopes in total. Next, we used ElliPro [ 31 ] to predict conformational epitopes, setting the screening parameters to a minimum score of 0.5 and a maximum distance of 6 Å. This ultimately yielded 28 candidate epitopes. The overlapping sequences from the ABCpred and ElliPro predictions were then identified and integrated based on the epitope length. For fully overlapping epitopes, the sequence predicted by ABCpred was adopted. For partially overlapping epitopes, the two sequence segments were fuzed to form a complete epitope covering both regions. Subsequently, we used VaxiJen [ 32 ] to analyze the antigenicity and ToxinPred2 [ 33 ] to evaluate their toxicity. Epitopes with a predicted antigenicity score exceeding 0.5 and lacking toxicity were selected for downstream applications. Owing to the scarcity of relevant data for epitope prediction, we leveraged the presumed similarity between the anchor residues of human HLA and porcine MHC class II haplotypes. Accordingly, NetMHCpanII‐4.1 [ 34 ] was employed to predict HTL epitopes (H2‐IAb, length(s): 15). Subsequently, VaxiJen was used to filter for antigenic candidates, selecting those with a score exceeding 0.4. For the prediction of CTL epitopes, the NetMHCpan‐4.1 tool [ 34 ] was applied to assess peptide binding to multiple SLA class I alleles, with the epitope length fixed at nine amino acids. The resulting candidates were further evaluated for antigenicity via VaxiJen, where epitopes scoring above 1.2 were prioritized. 2.2. Vaccine Development and Evaluation The epitopes were concatenated using AAY, EAAAK, KK, and GPGPG as linkers. Subsequently, the CDCRGDCFC peptide was conjugated to the epitope string via the flexible EAAAK linker, resulting in a protein designated as Pep. A three‐dimensional structural model of Pep was then predicted in silico using AlphaFold2 [ 35 ]. Using ChimeraX [ 36 ], we mapped the selected dominant epitopes onto the S protein structure (PDB ID: 6U7K) to visualize their distribution. We performed molecular docking of Pep (PDB ID: 7C77) with Toll‐like receptor 3 (TLR3) using ClusPro [ 37 ], with the resulting interactions visualized via LigPlot+. Subsequently, the immunogenicity of Pep was simulated using C‐ImmSim [ 38 ]. Molecular dynamics (MD) simulations of the complex were performed using iMODS [ 39 ]. 2.3. Plasmid Construction Previously established methods [ 21 ] were followed for constructing the pRbSoc plasmid. After codon optimization of the designed vaccine Pep, Xho I and Hin dIII restriction sites were inserted at either end of the gene. The gene fragment (Table 1 ) was then synthesized by Sangon Biotech and cloned into the pET‐28a and pRbSoc plasmids, resulting in the construction of the pET‐Pep and pRbSoc‐Pep plasmids. Table 1 RB69 Soc sequences. Name Nucleotide sequences (5′ to 3′) RB69 Soc

AAGCTT ACCACTTACTGGTGTAGGGGTAAACATTGCAGCGTTCTTAGTACGCCAATCTGCTGCGTCAGTCACCACAGTAGTGTAAGCAGCTTTTTCAGATGGGAAAGTCTGATAATGAGCATCAGCAATCCGATGTTCGTTTGAATAAATCTCAAACGGTACAGAAACTTCCATACCTTTAACTTCTTTACCTTCACCAGCAGGATGCGTAAAGGTTTTGATGTTTACATAACCACC GGATCC

Pep AAGCTT TGCGACTGCCGTGGTGACTGCTTCTGCGAAGCTGCTGCTAAAGAACACTCTGTTGTTGGTATCACCTGGGAAGCTGCTGCTAAATCTATGTCTATCCGTACCGAATACCTGGAAGCTGCTGCTAAATCTAAATTCAACGTTCAGGCTCCGGCTGTTGTTGTTCTGGGTGGTGGTCCGGGTCCGGGTAAATTCAACGTTCAGGCTCCGGCTGTTGTTGTTCTGGGTGGTTACGGTCCGGGTCCGGGTCTGGGTGTTTCTGTTTACGACCCGGCTTCTGGTCGTGTTGTTCAGAAAAAAAAAGACTGGTCTCGTGTTGCTACCAAATGCTACAACTCTGGTGGTTGCGCTGCTGCTTACAACGTTACCAACTCTTACGGTTACGTTTACAAATCTCAGGACTCTAACGGTCCGGGTCCGGGTCCGTCTTTCAACGACCACTCTTTCGTTAACATCACCGTTTCTGCTTCTTTCGGTGGTCACTCTGGTGCTAACCTGATCGCT CTCGAG

Note: The underlines indicate the introduced restriction enzyme sites of XhoⅠ and Hind Ⅲ. 2.4. Expression and Purification of Proteins Following previously established methods [ 21 ], protein expression was induced with IPTG for 7 h at 37°C. 2.5. Western Blotting Following electrophoretic separation, the proteins were electrotransferred onto a PVDF membrane. We blocked the membrane overnight at 4°C in 5% (w/v) skim milk in TBST (prepared by adding 0.1% Tween‐20 to Tris‐buffered saline) and then washed it with TBST. The membrane was then treated with 1:5000 diluted PEDV‐positive mouse serum for 1 h at 37°C. Subsequently, the membrane was rinsed thrice using TBST buffer, applied 1:5000‐diluted HRP‐conjugated anti‐mouse IgG (GAM‐HRP) (Abcam, UK), and conducted incubation with mild shaking for 1 h. 2.6. Preparation and Purification of T4 Soc − Phage T4 phage was prepared by infecting logarithmic‐phase E. coli P301 at an MOI of 0.1 and incubating overnight. The culture was centrifuged at 35,000  g for 35 min, then resuspended it in 10 mL of phosphate‐buffered saline (PBS) containing 600 μL of chloroform (shook the suspension at 4°C for 35 min). A subsequent centrifugation step at 5600  g for 18 min was performed to remove chloroform, yielding the purified phage preparation. 2.7. In Vitro Assembly of T4‐Pep Vaccine Soc‐Pep and T4 Soc − were conjugated using the previously described method [ 21 ]. To maximize the Pep display, T4 Soc − and Soc‐Pep were mixed at various molar ratios and incubated at 4°C for 55 min. The sample was subjected to centrifugation at 35,000  g for 40 min to remove any free Soc‐Pep. Next, the T4‐Pep phage was resuspend in PBS at a pH of 7.4. The number of copies was calculated using the previously described method [ 21 ]. 2.8. Mouse Immunizations and Challenges Female mice of the BALB/C were organized into four groups, as shown in Table 2 , and received oral vaccinations at weeks 0, 2, 4, and 6. The T4‐Pep and Pep groups were inoculated with an equal amount of Pep protein, respectively. The Pep concentration in the T4‐Pep group was calculated using the following formula: the product of 50 μg and Avogadro’s constant, divided by the molecular weight of Pep, and finally divided by the number of copies. Mouse serum was collected 14 days after each immunization. On day 15 after the third boost, all mice were orally inoculated with 100 TCID 50 of the PEDV‐CHN/SH‐2012‐5/2012 virus (the mice’s weight was recorded daily). CHN/SH‐2012‐5/2012 was maintained in our laboratory. Table 2 Grouping for mouse immunization. Group Dose (μL) PBS ( n  = 9) 100 T4 ( n  = 9) 100 T4 Pep ( n  = 9) 100 Pep ( n  = 9) 100 2.9. Specific Antibody Detection The PEDV antigen originates from a strain of PEDV‐CHN/SH‐2012‐5/2012 preserved in our laboratory. Plates coated overnight (4°C) with 100 ng/well PEDV were blocked with 2.5% skim milk (2 h, 37°C). After PBST washes, serially diluted sera (1:200–1:51,200) were added. Then, GAM‐HRP (1:5000) was applied and incubated under the same conditions for an additional hour. Following six PBST washes, TMB substrate (Solarbio, Beijing, China) was applied for 15 min at 37°C. The reaction was stopped with 5% H 2 SO 4 and the OD 450 was measured. 2.10. Serum Neutralization Assay Serum neutralizing antibodies against PEDV were determined by a virus neutralization assay. After heat‐inactivating (56°C, 30 min) the collected serum, a two‐fold serial dilution was performed and incubated with 100 TCID 50 of PEDV at 37°C for 1 h. The samples were loaded into 96‐well plates preseeded with Vero cell monolayers, followed by 1 h incubation at 37°C, and the supernatant was discarded. The cells were maintained in Dulbecco’s Modified Eagle Medium (serum‐free) and monitored daily for the development of cytopathic effects (CPEs). 2.11. Hematoxylin and eosin (HE) Staining Proximal jejunal segments collected at 7 days post‐challenge, approximately 4–5 cm distal to the pylorus, were fixed in 4% paraformaldehyde for 48 h. Gradient ethanol dehydration, paraffin embedding, and sectioning were performed on collected tissues, followed by routine HE staining. 2.12. Quantitative Real‐Time Reverse Transcription PCR (qRT‐PCR) Viral load in the proximal jejunal tissue was determined by qRT‐PCR. Total RNA was extracted from approximately 1 g of jejunal tissue using an RNA extraction kit (Accurate Biology, China). Reverse transcription was conducted to generate the cDNA. For amplification, we employed primers targeting the PEDV N gene (F: 5′‐AAAGGAAATAAGGACCAGCA‐3′ and R: 5′ ′ ‐AAATGCCAATTGGAAGGTTG‐3′ ′ ). The N‐protein cDNA sequence was cloned into PUC19 to create the PUC19‐N plasmid. After determining the concentration with a Nano‐100 Micro‐Spectrophotometer (Beyotime, China), the copy number concentration was calculated based on the molecular weight and Avogadro’s constant. Then, a 10‐fold gradient dilution (10 2 –10 8 copies/μL) was prepared to create a standard curve. Standard curves were used to measure the absolute copy number of viral RNA. 2.13. Statistical Analysis GraphPad Prism 8.0.2 was adopted for statistical analysis, with all data displayed as mean ± SD. 3. Results 3.1. Epitope Vaccine Design for PEDV The PEDV S protein was selected as the target antigen for epitope discovery because it is the principal surface glycoprotein involved in host‐cell entry [ 40 ]. Transmembrane‐topology analysis showed that amino acids 19–1326 lack transmembrane segments, indicating that this region is suitable for epitope screening (Figure 1 a).To improve screening reliability, linear and conformational epitopes were predicted using multiple bioinformatics tools, including ABCpred, ElliPro, NetMHCIIpan‐4.1 and NetMHCpan‐4.1. The S protein structure (Figure 1 b) used for conformational epitope prediction was retrieved from the PDB (PDB ID: 6U7K). As shown in Table 3 , none of these screened epitopes were found to be toxic. The outer surface of the S protein structure is where these epitopes are exposed, according to spatial analysis (Figure 1 d). The majority of these epitopes are located within the S1 region (Figure 1 c and Table 3 ). To assess epitope conservation, we retrieved S protein sequences from various PEDV strains in the NCBI database, including the highly pathogenic G2c (AHCZO2) [ 6 ]. Sequence alignment revealed over 91% similarity among the analyzed strains, with the identified linear epitopes being highly conserved across them (Figure 1 e). These epitopes were conjugated in a specific sequence using EAAAK, KK, AAY, and GPGPG linkers. In addition, we added a peptide segment (CDCRGDCFC), which is capable of binding to αvβ3 integrin [ 41 ], to the C‐terminus. This should enhance the vaccine’s targeting ability. Figure 1 In silico analysis and epitope screening of the PEDV S protein for vaccine design. (a) Predicted transmembrane topology of the PEDV S protein. (b) Three‐dimensional structure of the S protein (PDB ID: 6U7K) used as a template for conformational epitope prediction. (c) Schematic domain architecture of the PEDV S protein, illustrating the boundaries of the S1 and S2 subunits and the extracellular localization of the 19–1326 region. (d) Surface distribution of the identified dominant epitopes on the S protein trimer (colored regions), with most epitopes mapping to the S1 domain. (e) Sequence conservation analysis of linear epitopes across representative PEDV strains. Multiple sequence alignment of S proteins, including the highly pathogenic G2c strain (AHCZO2), revealed high epitope conservation. (f) Different epitope sequences were linked together using peptide linkers. Table 3 Candidate epitopes. Type Name Epitope Antigenicity Toxic Position BCL BCL1 LGVSVYDPASGRVVQK 0.5620 > 0.5 Nontoxic 878–893 BCL BCL2 DWSRVATKCYNSGGCA 0.9787 > 0.5 Nontoxic 188–203 BCL BCL3 NVTNSYGYVYKSQDSN 0.5069 > 0.5 Nontoxic 556–571 BCL BCL4 PSFNDHSFVNITVSASFGGHSGANLIA 0.6834 > 0.5 Nontoxic 505–531 CTL CTL1 EHSVVGITW 1.5570 > 1.2 Nontoxic 160–168 CTL CTL2 SMSIRTEYL 1.3770 > 1.2 Nontoxic 789–792 HTL HTL1 SKFNVQAPAVVVLGG 0.4039 > 0.4 Nontoxic 37–51 HTL HTL2 KFNVQAPAVVVLGGY 0.4278 > 0.4 Nontoxic 38–52 3.2. Candidate Vaccine Modeling and TLR3 Molecular Docking Following sequential linkage of the selected epitopes, the resulting multi‐epitope construct was termed Pep. Its three‐dimensional conformation was predicted via AlphaFold 2, as illustrated in Figure 2 a. To this end, the vaccine candidate must effectively engage immune receptors on target cells. Given that TLR3 targeting agents have been proven to boost vaccine potency by compensating for insufficient interferon secretion and protecting against highly pathogenic PEDV infection [ 42 ], we evaluated the interaction between our designed Pep and TLR3. Pep and TLR3 were designated as ligand and receptor, respectively. The resulting docked complex was analyzed using LigPlot+, as shown in Figure 2 b. Under the predicted binding mode, Pep formed stable interactions with TLR3, with key hydrogen bonds involving Pep residues Glu38, Tyr36, Glu35, Ser31, and Arg33. To further assess the dynamic stability of the Pep‐TLR3 complex, MD simulations were conducted using iMODS. Deformability analysis (Figure 2 c) revealed that most peaks were below 0.5, indicating that the backbone residues in this region are resistant to deformation and contribute to a compact structural conformation. The calculated eigenvalue for the complex was 2.234809 × 10 −6 (Figure 2 d), reflecting high rigidity and global stability. The covariance matrix (Figure 2 e) illustrated the coupling patterns between residue pairs. Additionally, the elastic network of the complex (Figure 2 f) showed dense gray regions at the binding interface, indicating strong interatomic interactions (stiffer springs). Collectively, these results demonstrate that the Pep‐TLR3 complex adopts a stable binding conformation with limited fluctuations, supporting its potential to effectively engage the immune receptor. Figure 2 In silico characterization and interaction analysis of the multi‐epitope vaccine construct Pep with TLR3. (a) Structure of the multi‐epitope vaccine candidate Pep, generated using AlphaFold 2. (b) Protein–protein docking analysis of the Pep‐TLR3 complex performed with the ClusPro server and visualized using LigPlot+. (c) Deformability analysis of the Pep‐TLR3 complex obtained from iMODS molecular dynamics simulations. (d) Eigenvalue plot showing the calculated eigenvalue of 2.234809 × 10 −6 , reflecting the high rigidity and global stability of the complex. (e) Covariance matrix illustrating the coupling patterns between residue pairs, where red, white, and blue represent correlated, uncorrelated, and anticorrelated motions, respectively. (f) Elastic network representation of the Pep‐TLR3 complex. Dense gray regions at the binding interface indicate strong interatomic interactions. 3.3. In Silico Assessment of Immune Activation Effects C‐ImmSim was used to simulate the immune response induced by the Pep construct after three rounds of antigen stimulation. The results demonstrated that following three rounds of antigenic stimulation, Pep effectively activated multiple immune cell populations, including B cells (Figure 3 d), natural killer (NK) cells (Figure 3 f), macrophages (Figure 3 c), and T cells (Figure 3 e). Notably, high levels of IgG antibodies were induced (Figure 3 a). Meanwhile, the concentrations of various cytokines remained consistently high (Figure 3 b). These findings suggest that Pep possesses strong immunogenic properties. Figure 3 C‐ImmSim‐based immunogenicity prediction of the Pep vaccine candidate. (a) Immunoglobulin profiles showing IgM and IgG antibody levels following three rounds of antigenic stimulation. (b) Cytokine and interleukin concentrations throughout the simulated immune response. (c) Macrophage dynamics, indicating activation upon antigen exposure. (d) B cell population dynamics, including total and memory B cells, reflecting a robust humoral response. (e) T cell population dynamics, depicting the expansion of helper and cytotoxic T lymphocytes. (f) NK cell dynamics, showing increased activity poststimulation. The epitope conservation analysis, structural protection prediction, and molecular docking results described above are intended solely to furnish a theoretical rationale and structural reference for the design of the multivalent vaccine molecules in this study. They do not constitute direct validation of the molecules’ biological immunogenicity. Further confirmation of the relevant immunogenicity and protective efficacy is required through subsequent experiments. 3.4. Construction of T4‐Pep Vaccine Since RB69 Soc protein enables efficient display of exogenous peptides at both terminals [ 23 ], this system was adopted to construct a T4 phage vaccine against PEDV. A fusion protein, Soc‐Pep, was generated by linking Pep to RB69 Soc, enabling Soc to anchor Pep onto the T4 phage capsid via Soc–T4 Soc − interactions (Figure 4 b). The expression vector for Soc‐Pep was constructed using the strategy depicted in Figure 4 a. High yields of Soc‐Pep were obtained in E. coli , and the proteins were purified (Figure 4 c). To optimize antigen loading, T4 Soc − (5 × 10 10 PFU) and Soc‐Pep were mixed at different molar ratios ranging from 1:1 to 32:1 (Figure 4 d). Image Pro Plus 6.0 grayscale analysis of protein bands was applied to quantify surface‐displayed Pep levels. As expected, Pep alone failed to bind T4 Soc − even at a 10:1 ratio (ctrl lane, Figure 4 d), confirming that binding is strictly Soc‐dependent. Display levels increased with the input ratio and reached saturation at approximately 16:1 (Figure 4 e). Based on these results, recombinant T4‐Pep was constructed. The Pep copy number per phage was calculated using the formula: copies = (Soc‐Pep grayscale value) × 49 × 930/(33 × (gp23  ∗ grayscale value)), yielding an average of approximately 850 copies per phage (Figure 4 e). Western blotting further confirmed that T4‐Pep was specifically recognized by PEDV‐positive mouse serum (Figure 4 f). Figure 4 Construction and characterization of the T4‐Pep nanoparticle vaccine. (a) Schematic diagram of the Soc‐Pep expression vector construction. (b) Illustration of the phage‐based antigen display strategy: the Soc‐Pep fusion protein is anchored onto Soc‐deficient T4 phage capsids through Soc–T4 Soc − interactions. (c) SDS‐PAGE analysis of purified Soc‐Pep and Pep proteins following expression in E. coli and affinity purification (M: marker, 1: Pep, 2: Soc‐Pep). (d) Coupling efficiency of T4 Soc − phage (5 × 10 10 PFU) with Soc‐Pep at various molar ratios of Pep to Soc binding sites (1:1–32:1). A control reaction using Pep alone at a 10:1 molar ratio (ctrl) confirmed the specificity of Soc‐mediated binding. (e) Grayscale quantification of gp23  ∗ and Soc‐Pep bands and calculation of the average Pep copy number displayed per T4 phage. (f) Western blot analysis confirming specific binding of Soc‐Pep to PEDV‐positive mouse serum (M: marker, 1: T4, 2: Soc‐Pep). 3.5. T4‐Pep Induces Robust Specific Antibody Production To evaluate the immunogenicity of the T4‐Pep vaccine, mice were immunized via oral gavage with 1.2 × 10 12 PFU T4‐Pep phage (equivalent to 50 μg of Pep), 50 μg of free Pep, T4, and PBS as a negative control (Table 2 ). The immunization regimen followed the schedule outlined in Figure 5 a. Serum was collected and PEDV‐specific antibody titers were quantified by ELISA. Mice immunized with free Pep produced only low levels of PEDV‐specific IgG compared with those immunized with T4‐Pep, which induced a significantly stronger antibody response (Figure 5 b). Notably, the T4‐Pep formulation induced high‐titer specific IgG antibodies, reaching a peak titer of 5 × 10 4 . At week 8, neutralizing antibody titers in the serum were assessed using a fixed virus dilution method. The T4‐Pep‐immunized group demonstrated higher neutralizing activity against live PEDV compared to the Pep‐alone group (Figure 5 c). Collectively, these findings demonstrate that the T4 phage nanoparticle platform exerts potent immunostimulatory effects. Figure 5 Immunogenicity evaluation of the T4‐Pep vaccine in mice. (a) Schematic diagram of the immunization schedule. Mice were immunized via oral gavage at weeks 0, 2, 4, and 6, with serum collected at weeks 2, 4, 6, and 8 postimmunization. (b) PEDV specific IgG antibody titers in serum samples collected at weeks 2, 4, 6, and 8 postimmunization, measured by ELISA ( n  = 3, all data were analyzed using a two‐tailed t ‐test). (c) Neutralizing antibody titers in week 8 serum samples determined by a fixed virus dilution method. Serial dilutions of immune mouse serum were incubated with PEDV, and neutralization titers were calculated as the reciprocal of the highest dilution showing complete neutralization ( n  = 3, all data were analyzed using a two‐tailed t ‐test). (ns, not significant;   ∗ p < 0.05;   ∗∗ p < 0.01;   ∗∗∗ p < 0.001). 3.6. T4‐Pep Provided Protection Against PEDV Challenge Subsequent to the completion of booster immunization, PEDV strain CHN/SH‐2012‐5/2012 was used to infect mice so as to explore the in vivo defense effect of T4‐Pep. Their body weight changes were then monitored for seven consecutive days. As shown in Figure 6 b, mice in theT4 and PBS groups exhibited progressive weight loss following viral challenge, whereas those immunized with T4‐Pep maintained relatively stable body weights throughout the monitoring period. On day 7 postinfection, intestinal tissue samples were collected for histopathological evaluation. HE staining revealed that the T4‐Pep‐immunized group displayed intact small intestinal villi with no significant pathological alterations, in contrast to the Pep, T4, and PBS‐immunized groups (Figure 6 a). Specifically, the T4‐ and PBS‐immunized groups showed marked villus atrophy and damage (red arrows, Figure 6 a, c), while the Pep‐only group exhibited mild villus injury and crypt hyperplasia (yellow arrows, Figure 6 a, c). Analysis of viral load in intestinal tissues revealed that the viral load in the tissues of mice vaccinated with the T4‐Pep vaccine was significantly lower than in those immunized with the Pep vaccine (Figure 6 d). Collectively, these results demonstrate that the T4 phage nanoparticle platform confers robust protection against PEDV infection in mice, effectively reducing viral replication and preserving intestinal integrity. Figure 6 Protective efficacy of Pep T4 against PEDV challenge in mice. (a) Representative histological images of mouse intestinal tissue (scale bar: 200 μm). Pathological alterations include villous injury (red arrows) and crypt hyperplasia (yellow arrows). (b) Daily body weight changes in mice over 7 days post‐PEDV infection ( n  = 6, all data were analyzed using a two‐tailed t ‐test). (c) Villus length measurements in the proximal jejunum ( n  = 6, all data were analyzed using a two‐tailed t ‐test). (d) Viral loads in the proximal jejunum of challenged and control mice, quantified by qRT‐PCR. ( n  = 3, all data were analyzed using a two‐tailed t ‐test). (ns, not significant;   ∗ p < 0.05;   ∗∗ p < 0.01;   ∗∗∗ p < 0.001;   ∗∗∗∗ p < 0.0001). 4. Discussion PEDV still poses a severe menace to the pig breeding industry worldwide, inflicting substantial economic losses across all age groups of pigs [ 43 ]. In China, recent large‐scale outbreaks of diarrhea have been reported in pig populations, with PEDV implicated as the primary viral etiology in 50.90% of cases and detected in 66.67% of affected farms [ 17 ]. Although commercial vaccines against PEDV are currently available, the continuous genetic evolution of circulating strains has compromised their effectiveness, highlighting the urgent need for novel vaccine platforms capable of conferring broad and durable protection [ 44 ]. In this study, we designed a multi‐epitope peptide derived from the PEDV S protein and constructed the T4‐Pep candidate vaccine using bacteriophage T4 nanoparticles as a delivery platform. This approach integrates immunoinformatic prediction, structural biology analysis, and nanotechnology to address the inherent limitations of low immunogenicity in traditional subunit vaccines and to assess the potential of oral immunization in inducing immune responses. Vaccination initiates a complex immune response. During this procedure, B cells mediate humoral immunity via antibody responses, while CTLs and HTLs are responsible for orchestrating cellular immunity, which is essential for clearing viruses [ 45 , 46 ]. The identification of viral epitopes capable of engaging these distinct lymphocyte populations is therefore fundamental to rational vaccine design. Immunoinformatic approaches have emerged as powerful tools for predicting protective antigenic epitopes and accelerating vaccine development [ 47 , 48 ]. The S protein was used as the target for screening vaccine epitopes in this study. Our analysis indicates that the region spanning amino acids 19–1326 is located in the extracellular domain. Further sequence alignment of S proteins from multiple PEDV strains, including the highly pathogenic G2c (AHCZO2) strain, revealed over 91.46% similarity, and the identified linear epitopes exhibited high conservation across these strains. This significant conservation suggests that vaccines based on these epitopes may provide cross‐protection against multiple PEDV variants, which is a key characteristic for addressing the ongoing circulation of emerging strains such as G2b and G2c. In this study, we employed immunoinformatic analysis to predict and screen immunodominant epitopes derived from the PEDV S protein, building upon established epitope prediction frameworks [ 21 ]. Beyond epitope selection, effective vaccine design must balance immunogenicity enhancement with acceptable reactogenicity and safety profiles [ 7 ]. To further assess vaccine‐receptor interactions, we performed molecular docking between the multi‐epitope construct (Pep) and TLR3 using the Cluspro server. TLR3 recognizes double‐stranded RNA intermediates generated during PEDV replication, thereby initiating host innate immune and interferon responses [ 49 ]. Nevertheless, upon cell infection, PEDV employs multiple viral proteins to inhibit the TLR3 signaling pathway and evade host immune surveillance [ 50 ]. Therefore, targeting TLR3 represents a key strategy to antagonize PEDV immune evasion and restore host antiviral defenses. Molecular docking can predict the binding affinity of vaccine peptides to TLR3, verifying whether the designed vaccine can effectively bind TLR3 at the structural level. Additionally, C‐ImmSim simulations were used to predict that the Pep construct would induce robust humoral and cellular immune responses. Despite their promise, epitope‐based vaccines face inherent limitations related to the weak immunogenicity of peptide antigens, necessitating efficient delivery platforms to potentiate immune activation. Recent advances in nanobiotechnology have reframed viruses not merely as pathogens but as functional nanoparticles with diverse biomedical applications, including vaccine delivery. Structural proteins from viruses including adeno‐associated virus (AAVs) [ 51 ] and bacteriophages [ 28 ] have been successfully engineered to produce vaccines. Of these platforms, bacteriophage T4 shows the most promise as a vaccine delivery system. In recent years, researchers have extensively explored novel strategies, such as subunit vaccines [ 12 ], viral vector vaccines [ 52 ], nucleic acid vaccines [ 53 ], and mucosal delivery systems [ 11 ], in an attempt to overcome the limitations of traditional vaccines when it comes to preventing and controlling PEDV. However, most of these novel vaccines still face challenges such as insufficient immunogenicity and limited antigen presentation efficiency [ 2 ]. Compared to other PEDV vaccine candidates, the T4‐Pep platform exhibits distinct immunological advantages. One recent investigation developed recombinant Lactobacillus paracasei to produce subunit vaccine candidates against PEDV [ 14 ]. Following oral immunization of pregnant mice with this recombinant strain, a gradual increase in PEDV‐specific antibody titers was observed in both serum and intestinal tissues over time. However, despite a statistically significant elevation compared to the control group, the overall antibody levels remained relatively modest. These findings suggest that immunization with the S1 protein alone may possess limited intrinsic immunogenicity, underscoring the potential benefit of multivalent display platforms such as T4‐Pep in enhancing humoral immune responses. Results demonstrated that equivalent Pep content delivered via the T4 carrier evoked higher serum IgG levels than separate Pep vaccination. These results indicate that the T4 phage delivery platform developed in this study specifically addresses these critical shortcomings in PEDV vaccine development. It demonstrates significant advantages in terms of antigen presentation efficiency and other aspects, providing a practical and feasible technical pathway for the development of novel vaccines that are better suited to the characteristics of PEDV infection and offer more stable protective effects. Although the candidate vaccine developed in this study shows great potential for application, several aspects warrant further investigation. First, this study used mice as an animal model rather than pigs, the natural host; therefore, the characteristics of the induced immune response and the actual protective efficacy still need to be further validated and evaluated in a porcine model. Second, this study did not conduct direct measurements of mucosal‐related indicators, making it difficult to fully reflect the body’s mucosal immune status. Future studies could incorporate mucosal site‐specific detection indicators to more systematically evaluate the vaccine’s immunogenicity. Furthermore, as this vaccine was designed based on antigenic epitopes rather than the full‐length antigen, the immune profile it induces differs somewhat from that of whole‐antigen immunization, and the underlying protective mechanisms require further elucidation. In conclusion, this study involved the development of a PEDV vaccine platform using the T4 bacteriophage as a vector and further assessed its ability to elicit immune reactions. In murine models, T4‐Pep exerted prominent protective effects against PEDV infection, hence serving as a highly prospective candidate vaccine for PEDV prevention. Author Contributions

GuoQing Zhao : conceptualization, validation, methodology, writing – original draft. ShiDan Zhang : methodology, validation, writing – review and editing. YuMin Zhang and ShengJing Jiao : validation. XiaoYan Zeng : formal analysis. LuRu Zhao : methodology. JingJiao Ma : investigation. YuQiang Cheng : visualization. HengAn Wang : supervision. YaXian Yan and JianHe Sun : funding acquisition. ZhaoFei Wang: project administration, conceptualization. Funding This research was funded by the Science and Technology Commission of Shanghai Municipality (Grant 23N51900300) and the National Natural Science Foundation of China (Grant 32373097). Disclosure All participants in this research have approved the finalized article. Ethics Statement The experimental procedures involving mice strictly adhered to the Guiding Principles in the Care and Use of Animals (China) and received approval by the Ethical Committee for Animal Experiments of Shanghai Jiao Tong University (China) (Approval Number 202201312). Conflicts of Interest The authors declare no conflicts of interest. Acknowledgments This research was funded by the Science and Technology Commission of Shanghai Municipality (Grant 23N51900300) and the National Natural Science Foundation of China (Grant 32373097). The authors gratefully acknowledge Professor Pan Tao from the College of Veterinary Medicine, Huazhong Agricultural University for kindly providing the T4 bacteriophage used in this study. Data Availability Statement The data that support the findings of this study are available upon request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. 1

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PMC10865985

📖 中文全文 Chinese Full Text

中文

以下为中文翻译(保留关键术语与缩写,专有名词、基因/蛋白名称、数据库及软件名称等按学术惯例保留英文或附注):

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**PMC;Transbound Emerg Dis;Transbound Emerg Dis 4732;tbed;TBED;《Transboundary and Emerging Diseases》(跨边界与新兴疾病);1865-1674;1865-1682;Wiley;PMC13266086;PMC13266086.1;13266086;13266086;42290005;10.1155/tbed/8438783;TBED8438783;1;研究论文;论文**

**基于T4噬菌体的猪流行性腹泻病毒多表位纳米颗粒疫苗的临床前评价**

Zhao GuoQing(赵国青) Zhang ShiDan(张诗丹) Zhang YuMin(张玉敏) Jiao ShengJing(焦圣静) Zeng XiaoYan(曾晓燕) Zhao LuRu(赵露露) Wang Jie(王杰) Ma JingJiao(马静娇) Cheng YuQiang(程玉强) Wang HengAn(王恒安) Yan YaXian(严亚仙) Sun JianHe(孙建和) Wang ZhaoFei(王兆飞) Chen Nan-hua(陈南华)

单位:上海交通大学农业与生物学院,上海市兽医生物技术重点实验室,中国上海,201100;sjtu.edu.cn

日期:2026年6月14日;2026年;2026年;503610;8438783;2026年5月19日;2026年3月11日;2026年5月21日;2026年6月14日;2026年6月16日;2026年6月17日

版权:© 2026 GuoQing Zhao 等。《Transboundary and Emerging Diseases》由 John Wiley & Sons Ltd 出版。2026年。本文依据 https://creativecommons.org/licenses/by/4.0/ 许可协议开放获取,该许可允许在任何媒介中使用、分发和复制,前提是适当引用原始作品。

**摘要** 猪流行性腹泻病毒(porcine epidemic diarrhea virus, PEDV)持续威胁全球养猪业,目前可用的疫苗往往无法对新兴强毒株提供完全保护。本研究开发了一种靶向PEDV的基于T4噬菌体的多表位纳米颗粒疫苗。通过免疫信息学分析鉴定了来源于PEDV刺突(spike, S)蛋白的B细胞和T细胞表位,并利用柔性连接肽将其组装为串联表位构建体(Pep)。计算机模拟分析预测Pep具有有利的抗原特性,且与Toll样受体3(Toll-like receptor 3, TLR3)之间存在稳定相互作用。重组Pep蛋白在大肠杆菌(*Escherichia coli*)中表达,随后展示于T4噬菌体表面,制备得到T4-Pep疫苗。表征结果显示,每个噬菌体携带约800拷贝Pep。在小鼠中,T4-Pep免疫诱导的PEDV特异性IgG水平和病毒中和抗体滴度显著高于Pep单独免疫。PEDV攻毒后,T4-Pep免疫小鼠表现出更好的保护效果,并减轻肠道损伤,组织病理学分析证实了这一点。综上,这些结果凸显了T4噬菌体作为高效且具有免疫原性的病毒表位递送平台的潜力,为开发针对PEDV及相关病原体的疫苗提供了有前景的策略。

**关键词**:表位;噬菌体;猪流行性腹泻病毒;疫苗

**资助项目**:上海市科学技术委员会(10.13039/501100003399;23N51900300);国家自然科学基金(10.13039/501100001809;32373097)

PMC状态:qastatus 0;live yes;embargo no;released yes;open-access yes;olf no;manuscript no;legally-suppressed no;has-pdf yes;has-supplement no;pdf-only no;suppress-copyright no;is-real-version no;is-scanned-article no;preprint no;in-epmc yes;license-ref CC BY;source-schema-version-number 2.0;cover-date 2026;出版商转换信息:Converter:WILEY_ML3GV2_TO_JATSPMC version:6.8.0 mode:remove_FC converted:15.06.2026

Zhao, GuoQing; Zhang, ShiDan; Zhang, YuMin; Jiao, ShengJing; Zeng, XiaoYan; Zhao, LuRu; Wang, Jie; Ma, JingJiao; Cheng, YuQiang; Wang, HengAn; Yan, YaXian; Sun, JianHe; Wang, ZhaoFei. 基于T4噬菌体的猪流行性腹泻病毒多表位纳米颗粒疫苗的临床前评价. 《Transboundary and Emerging Diseases》, 2026, 8438783, 13页, 2026. 10.1155/tbed/8438783. 42290005.

GuoQing Zhao 和 ShiDan Zhang 对本工作贡献相同。 学术编辑:Nan-hua Chen

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## 1. 引言

猪流行性腹泻病毒(PEDV)主要通过粪-口途径传播,并主要感染动物肠道。哺乳仔猪对PEDV感染尤为易感。感染后死亡率可达50%至100%。该病毒对肠上皮细胞具有明显嗜性,可诱导严重绒毛萎缩,最终导致吸收不良性腹泻、脱水乃至死亡。尽管传统疫苗已用于预防PEDV,但其对新兴变异株的防护效果并不理想。疫苗接种后,细胞会触发一系列复杂的免疫应答。病毒感染细胞主要通过细胞毒性T淋巴细胞(cytotoxic T lymphocytes, CTL)介导的免疫应答被清除。同时,辅助性T细胞表位(helper T lymphocyte epitopes, HTL)可促进B细胞活化与分化,从而产生抗体。利用免疫信息学工具预测B细胞和T淋巴细胞表位,已显著加快了抗病毒疫苗的设计与开发。

目前,针对PEDV的疫苗研究涵盖多种技术路线,包括PEDV弱毒活疫苗和灭活疫苗;基于阳离子脂质体的口服PEDV疫苗;亚单位疫苗;纳米颗粒疫苗;以及脂质纳米颗粒包裹的mRNA PEDV疫苗等。然而,PEDV在外界压力下不断进化与突变,使其防控难度日益增加,PEDV仍难以被有效遏制。目前,基于表位的疫苗已成为一类有前景的免疫原,尤其在兽医学领域。含有明确病毒表位的亚单位疫苗为传统方法提供了有吸引力的替代方案,兼具更高的安全性特征和精准免疫靶向能力。

PEDV的刺突(S)蛋白介导病毒吸附与膜融合,是中和抗体的主要靶标,并包含多种对保护性免疫至关重要的免疫显性B细胞和T细胞表位。然而,仅肽类抗原通常免疫原性较弱,需要高效的递送系统或免疫刺激佐剂才能诱发充分免疫应答。T4噬菌体近期已被用于疫苗开发,其方式是将抗原展示于其衣壳表面。T4噬菌体已成为一种多功能且高度免疫原性的疫苗平台。其表面结构包含两种非必需衣壳蛋白——Soc和Hoc,可通过基因融合或化学偶联方式展示异源肽。研究表明,T4噬菌体载体本身即可增强免疫应答。此外,T4噬菌体衣壳蛋白的重复且对称排列方式类似于可激活模式识别受体(pattern recognition receptors, PRRs)的人类病毒病原相关分子模式(pathogen-associated molecular patterns, PAMPs)。这些特征可能结合细胞外PRRs,触发炎症信号传导。此外,T4噬菌体主要衣壳蛋白数量庞大,可使抗原以浓缩方式整合入噬菌体。这种多价展示可强烈激活B细胞受体,从而诱导强烈的体液免疫应答。该特性还可能通过调节抗原拷贝数和间距来优化免疫原性。

通过利用噬菌体的固有免疫刺激特性,基于噬菌体的疫苗平台可规避传统疫苗方法的诸多局限,增强靶抗原的免疫原性。此外,噬菌体本身也可诱导免疫应答。近年来,噬菌体递送系统的进展为商业化疫苗开发开辟了新途径。综合来看,这些进展支持探索新型噬菌体载体疫苗用于PEDV防控,作为减轻疫情爆发的有前景策略。越来越多的证据表明,T4噬菌体作为抗病毒疫苗平台具有巨大潜力。本研究利用生物信息学方法鉴定PEDV S蛋白中的表位,随后通过体外组装方法将这些表位串联并展示于T4噬菌体上。对其性质和免疫原性的后续评价表明,该构建体有望成为疫苗候选分子,为PEDV防控提供理论和实践依据。

---

## 2. 材料与方法

### 2.1 表位预测

以PEDV S蛋白(GenBank: AVK78141.1)作为表位预测模板。同时,从NCBI数据库获取不同基因型PEDV的S蛋白序列,并使用ESPript 3.2进行比对分析。采用ABCpred预测16个残基长度、阈值为0.85的B细胞表位(B-cell epitopes, BCL),共获得29个候选表位。随后,使用ElliPro预测构象表位,筛选参数设置为最低得分0.5、最大距离6 Å,最终获得28个候选表位。然后,根据表位长度识别并整合ABCpred与ElliPro预测结果中的重叠序列。对于完全重叠的表位,采用ABCpred预测的序列;对于部分重叠的表位,将两段序列融合,形成覆盖两个区域的完整表位。随后,使用VaxiJen分析抗原性,并使用ToxinPred2评估毒性。选择预测抗原性得分大于0.5且无毒性的表位用于后续应用。

由于表位预测相关数据有限,本研究利用人类HLA锚定残基与猪MHC II类单倍型之间假定相似性。因此,采用NetMHCpanII-4.1预测HTL表位(H2-IAb,长度:15)。随后,使用VaxiJen筛选具有抗原性的候选表位,选择得分大于0.4者。对于CTL表位预测,采用NetMHCpan-4.1工具评估肽段与多种SLA I类等位基因的结合能力,表位长度固定为9个氨基酸。所得候选表位进一步通过VaxiJen评估抗原性,优先选择得分高于1.2的表位。

### 2.2 疫苗开发与评价

使用AAY、EAAAK、KK和GPGPG作为连接肽将各表位串联。随后,通过柔性EAAAK连接肽将CDCRGDCFC肽段偶联至表位串联序列,得到命名为Pep的蛋白。随后,使用AlphaFold2对Pep进行三维结构模型预测。使用ChimeraX将所选显性表位映射至S蛋白结构(PDB ID: 6U7K)上,以可视化其分布。使用ClusPro对Pep(PDB ID: 7C77)与Toll样受体3(TLR3)进行分子对接,并使用LigPlot+可视化相互作用。随后,使用C-ImmSim模拟Pep的免疫原性。使用iMODS对复合物进行分子动力学(molecular dynamics, MD)模拟。

### 2.3 质粒构建

按照既往建立的方法构建pRbSoc质粒。对设计疫苗Pep进行密码子优化后,在基因两端分别插入Xho I和Hind III限制性酶切位点。随后,由生工生物(Sangon Biotech)合成基因片段(表1),并将其克隆至pET-28a和pRbSoc质粒中,分别构建pET-Pep和pRbSoc-Pep质粒。

**表1 RB69 Soc序列**

| 名称 | 核苷酸序列(5′至3′) | |---|---| | RB69 Soc | AAGCTT ACCACTTACTGGTGTAGGGGTAAACATTGCAGCGTTCTTAGTACGCCAATCTGCTGCGTCAGTCACCACAGTAGTGTAAGCAGCTTTTTCAGATGGGAAAGTCTGATAATGAGCATCAGCAATCCGATGTTCGTTTGAATAAATCTCAAACGGTACAGAAACTTCCATACCTTTAACTTCTTTACCTTCACCAGCAGGATGCGTAAAGGTTTTGATGTTTACATAACCACC GGATCC | | Pep | AAGCTT TGCGACTGCCGTGGTGACTGCTTCTGCGAAGCTGCTGCTAAAGAACACTCTGTTGTTGGTATCACCTGGGAAGCTGCTGCTAAATCTATGTCTATCCGTACCGAATACCTGGAAGCTGCTGCTAAATCTAAATTCAACGTTCAGGCTCCGGCTGTTGTTGTTCTGGGTGGTGGTCCGGGTCCGGGTAAATTCAACGTTCAGGCTCCGGCTGTTGTTGTTCTGGGTGGTTACGGTCCGGGTCCGGGTCTGGGTGTTTCTGTTTACGACCCGGCTTCTGGTCGTGTTGTTCAGAAAAAAAAAGACTGGTCTCGTGTTGCTACCAAATGCTACAACTCTGGTGGTTGCGCTGCTGCTTACAACGTTACCAACTCTTACGGTTACGTTTACAAATCTCAGGACTCTAACGGTCCGGGTCCGGGTCCGTCTTTCAACGACCACTCTTTCGTTAACATCACCGTTTCTGCTTCTTTCGGTGGTCACTCTGGTGCTAACCTGATCGCT CTCGAG |

注:下划线表示引入的Xho I和Hind III限制性酶切位点。

### 2.4 蛋白表达与纯化

按照既往建立的方法,使用IPTG在37°C诱导蛋白表达7小时。

### 2.5 Western blotting

电泳分离后,将蛋白电转至PVDF膜上。将膜置于含5%(w/v)脱脂奶粉的TBST中(TBST为在Tris缓冲盐水中加入0.1% Tween-20配制),4°C封闭过夜,随后用TBST洗涤。将膜与1:5000稀释的PEDV阳性小鼠血清37°C孵育1小时。随后,用TBST缓冲液洗涤三次,加入1:5000稀释的HRP标记抗小鼠IgG(GAM-HRP,Abcam,英国),轻柔摇动孵育1小时。

### 2.6 T4 Soc⁻噬菌体的制备与纯化

通过以MOI 0.1感染对数生长期的*E. coli* P301并过夜培养来制备T4噬菌体。将培养物以35,000 g离心35分钟,随后重悬于含600 μL氯仿的10 mL磷酸盐缓冲液(PBS)中(4°C振荡悬浮液35分钟)。随后以5600 g离心18分钟以去除氯仿,获得纯化的噬菌体制剂。

### 2.7 T4-Pep疫苗体外组装

按照既往描述的方法将Soc-Pep与T4 Soc⁻偶联。为最大化Pep展示,将T4 Soc⁻与Soc-Pep按不同摩尔比例混合,4°C孵育55分钟。将样品以35,000 g离心40分钟,以去除游离Soc-Pep。随后,将T4-Pep噬菌体重悬于pH 7.4的PBS中。拷贝数按照既往描述的方法计算。

### 2.8 小鼠免疫与攻毒

将BALB/C雌性小鼠分为四组(表2),并在第0、2、4和6周进行口服免疫。T4-Pep组和Pep组分别接种等量的Pep蛋白。T4-Pep组中Pep浓度按以下公式计算:50 μg与阿伏伽德罗常数的乘积,除以Pep分子量,再除以拷贝数。每次免疫后14天采集小鼠血清。第三次加强免疫后第15天,所有小鼠口服接种100 TCID₅₀的PEDV-CHN/SH-2012-5/2012病毒(每日记录小鼠体重)。该毒株由本实验室保种。

**表2 小鼠免疫分组**

| 组别 | 剂量(μL) | |---|---:| | PBS(n = 9) | 100 | | T4(n = 9) | 100 | | T4 Pep(n = 9) | 100 | | Pep(n = 9) | 100 |

### 2.9 特异性抗体检测

PEDV抗原来源于本实验室保种的PEDV-CHN/SH-2012-5/2012毒株。将酶标板以每孔100 ng PEDV抗原4°C包被过夜,随后用2.5%脱脂奶粉37°C封闭2小时。PBST洗涤后,加入梯度稀释血清(1:200–1:51,200)。随后加入GAM-HRP(1:5000),在相同条件下再孵育1小时。经六次PBST洗涤后,加入TMB底物(Solarbio,中国北京),37°C显色15分钟。用5% H₂SO₄终止反应,并测定OD₄₅₀。

### 2.10 血清中和试验

通过病毒中和试验检测血清中针对PEDV的中和抗体。将采集的血清56°C热灭活30分钟后,进行两倍系列稀释,并与100 TCID₅₀ PEDV在37°C孵育1小时。将样品加入预先铺有Vero细胞单层96孔板中,37°C孵育1小时后弃去上清。细胞用无血清Dulbecco改良鹰氏培养基维持,并每日观察细胞病变效应(cytopathic effects, CPEs)。

### 2.11 苏木精-伊红(HE)染色

攻毒后第7天采集近端空肠组织段,约位于幽门远端4–5 cm处,固定于4%多聚甲醛中48小时。对采集组织进行梯度乙醇脱水、石蜡包埋和切片,随后进行常规HE染色。

### 2.12 定量实时逆转录PCR(qRT-PCR)

通过qRT-PCR检测近端空肠组织中的病毒载量。使用RNA提取试剂盒(Accurate Biology,中国)从约1 g空肠组织中提取总RNA。进行逆转录生成cDNA。扩增采用靶向PEDV N基因的引物(F:5′-AAAGGAAATAAGGACCAGCA-3′;R:5′-AAATGCCAATTGGAAGGTTG-3′)。将N蛋白cDNA序列克隆至PUC19中,构建PUC19-N质粒。使用Nano-100微量分光光度计(Beyotime,中国)测定浓度后,根据分子量和阿伏伽德罗常数计算拷贝数浓度。随后制备10倍梯度稀释(10²–10⁸ copies/μL)以建立标准曲线。利用标准曲线测定病毒RNA绝对拷贝数。

### 2.13 统计分析

采用GraphPad Prism 8.0.2进行统计分析,所有数据以均值 ± 标准差表示。

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## 3. 结果

### 3.1 PEDV表位疫苗设计

选择PEDV S蛋白作为表位发现的目标抗原,因为它是参与宿主细胞进入的主要表面糖蛋白。跨膜拓扑分析显示,第19–1326位氨基酸缺乏跨膜区段,表明该区域适合表位筛选(图1a)。为提高筛选可靠性,使用多种生物信息学工具预测线性表位和构象表位,包括ABCpred、ElliPro、NetMHCIIpan-4.1和NetMHCpan-4.1。用于构象表位预测的S蛋白结构(图1b)取自PDB(PDB ID: 6U7K)。如表3所示,这些筛选所得表位均未发现毒性。空间分析显示,这些表位暴露于S蛋白结构外表面(图1d)。这些表位中的大多数位于S1区域(图1c和表3)。

为评估表位保守性,从NCBI数据库检索不同PEDV毒株的S蛋白序列,包括高致病性G2c毒株(AHCZO2)。序列比对显示,所分析毒株间相似度超过91%,且鉴定所得线性表位在这些毒株中高度保守(图1e)。这些表位使用EAAAK、KK、AAY和GPGPG连接肽按特定顺序连接。此外,在C端添加肽段CDCRGDCFC,该肽段可结合αvβ3整合素,以增强疫苗靶向能力。

**图1 PEDV S蛋白用于疫苗设计的计算机模拟分析与表位筛选。** (a) PEDV S蛋白预测跨膜拓扑结构。 (b) 用于构象表位预测的S蛋白三维结构(PDB ID: 6U7K)。 (c) PEDV S蛋白结构域架构示意图,显示S1和S2亚单位边界以及19–1326区域的胞外定位。 (d) 鉴定所得显性表位在S蛋白三聚体表面的分布(彩色区域),大多数表位映射至S1结构域。 (e) 代表性PEDV毒株间线性表位序列保守性分析。S蛋白多序列比对,包括高致病性G2c毒株(AHCZO2),显示表位高度保守。 (f) 不同表位序列通过肽连接肽连接。

**表3 候选表位**

| 类型 | 名称 | 表位 | 抗原性 | 毒性 | 位置 | |---|---|---|---:|---|---| | BCL | BCL1 | LGVSVYDPASGRVVQK | 0.5620 > 0.5 | 非毒性 | 878–893 | | BCL | BCL2 | DWSRVATKCYNSGGCA | 0.9787 > 0.5 | 非毒性 | 188–203 | | BCL | BCL3 | NVTNSYGYVYKSQDSN | 0.5069 > 0.5 | 非毒性 | 556–571 | | BCL | BCL4 | PSFNDHSFVNITVSASFGGHSGANLIA | 0.6834 > 0.5 | 非毒性 | 505–531 | | CTL | CTL1 | EHSVVGITW | 1.5570 > 1.2 | 非毒性 | 160–168 | | CTL | CTL2 | SMSIRTEYL | 1.3770 > 1.2 | 非毒性 | 789–792 | | HTL | HTL1 | SKFNVQAPAVVVLGG | 0.4039 > 0.4 | 非毒性 | 37–51 | | HTL | HTL2 | KFNVQAPAVVVLGGY | 0.4278 > 0.4 | 非毒性 | 38–52 |

### 3.2 候选疫苗建模与TLR3分子对接

将所选表位依次连接后,所得多表位构建体命名为Pep。其三维构象通过AlphaFold2预测,如图2a所示。为此,疫苗候选分子必须能有效结合靶细胞上的免疫受体。鉴于TLR3靶向剂已被证明可通过补偿干扰素分泌不足来增强疫苗效力,并保护机体免受高致病性PEDV感染,本研究评估了所设计Pep与TLR3之间的相互作用。将Pep和TLR3分别设为配体和受体。所得对接复合物使用LigPlot+分析,如图2b所示。在预测结合模式下,Pep与TLR3形成稳定相互作用,关键氢键涉及Pep残基Glu38、Tyr36、Glu35、Ser31和Arg33。

为进一步评估Pep-TLR3复合物的动态稳定性,使用iMODS进行分子动力学模拟。可变形性分析(图2c)显示,大多数峰值低于0.5,表明该区域骨架残基抗变形,有助于形成紧凑结构构象。计算所得复合物特征值为2.234809 × 10⁻⁶(图2d),反映其高刚性和整体稳定性。协方差矩阵(图2e)展示了残基对之间的耦合模式。此外,复合物弹性网络(图2f)显示结合界面处存在密集灰色区域,表明强原子间相互作用(更硬的弹簧)。综合来看,这些结果表明Pep-TLR3复合物采取稳定结合构象且波动有限,支持其有效结合免疫受体的潜力。

**图2 多表位疫苗构建体Pep与TLR3的计算机模拟表征及相互作用分析。** (a) 使用AlphaFold2生成的多表位疫苗候选分子Pep结构。 (b) 使用ClusPro服务器进行Pep-TLR3复合物蛋白-蛋白对接分析,并使用LigPlot+可视化。 (c) 基于iMODS分子动力学模拟获得的Pep-TLR3复合物可变形性分析。 (d) 特征值图,显示计算所得特征值2.234809 × 10⁻⁶,反映复合物高刚性和整体稳定性。 (e) 协方差矩阵,展示残基对之间的耦合模式,其中红色、白色和蓝色分别代表相关、不相关和反相关运动。 (f) Pep-TLR3复合物弹性网络表示。结合界面处密集灰色区域表明强原子间相互作用。

### 3.3 免疫激活效应的计算机模拟评估

使用C-ImmSim模拟Pep构建体经三轮抗原刺激后诱导的免疫应答。结果显示,经三轮抗原刺激后,Pep有效激活多种免疫细胞群,包括B细胞(图3d)、自然杀伤(natural killer, NK)细胞(图3f)、巨噬细胞(图3c)和T细胞(图3e)。值得注意的是,诱导了高水平IgG抗体(图3a)。同时,多种细胞因子浓度持续保持较高水平(图3b)。这些发现提示Pep具有较强免疫原性。

**图3 基于C-ImmSim的Pep疫苗候选分子免疫原性预测。** (a) 经三轮抗原刺激后IgM和IgG抗体水平的免疫球蛋白谱。 (b) 模拟免疫应答过程中细胞因子和白细胞介素浓度。 (c) 巨噬细胞动态变化,显示抗原暴露后活化。 (d) B细胞群体动态变化,包括总B细胞和记忆B细胞,反映强烈体液免疫应答。 (e) T细胞群体动态变化,显示辅助性T淋巴细胞和细胞毒性T淋巴细胞扩增。 (f) NK细胞动态变化,显示刺激后活性增加。

上述表位保守性分析、结构保护性预测和分子对接结果,仅用于为本研究中多价疫苗分子设计提供理论依据和结构参考,并不构成对分子生物学免疫原性的直接验证。相关免疫原性和保护效力仍需通过后续实验进一步确认。

### 3.4 T4-Pep疫苗构建

由于RB69 Soc蛋白可在两端高效展示外源肽,本研究采用该系统构建抗PEDV的T4噬菌体疫苗。通过将Pep与RB69 Soc连接,生成融合蛋白Soc-Pep,使Soc能够通过Soc–T4 Soc⁻相互作用将Pep锚定于T4噬菌体衣壳上(图4b)。Soc-Pep表达载体按照图4a所示策略构建。在*E. coli*中获得高表达量的Soc-Pep,并对蛋白进行纯化(图4c)。为优化抗原装载,将T4 Soc⁻(5 × 10¹⁰ PFU)与Soc-Pep按1:1至32:1的不同摩尔比例混合(图4d)。使用Image Pro Plus 6.0对蛋白条带进行灰度分析,以定量表面展示Pep水平。如预期,即使按10:1比例,Pep单独仍不能结合T4 Soc⁻(ctrl泳道,图4d),证实结合严格依赖Soc。展示水平随加入比例增加而升高,并在约16:1时达到饱和(图4e)。基于这些结果,构建重组T4-Pep。每个噬菌体Pep拷贝数按以下公式计算:copies =(Soc-Pep灰度值)× 49 × 930 /(33 ×(gp23*灰度值)),平均每个噬菌体约850拷贝(图4e)。Western blotting进一步证实T4-Pep可被PEDV阳性小鼠血清特异性识别(图4f)。

**图4 T4-Pep纳米颗粒疫苗构建与表征。** (a) Soc-Pep表达载体构建示意图。 (b) 基于噬菌体的抗原展示策略示意图:Soc-Pep融合蛋白通过Soc–T4 Soc⁻相互作用锚定于Soc缺陷型T4噬菌体衣壳上。 (c) *E. coli*表达及亲和纯化后纯化的Soc-Pep和Pep蛋白SDS-PAGE分析(M:marker;1:Pep;2:Soc-Pep)。 (d) T4 Soc⁻噬菌体(5 × 10¹⁰ PFU)与Soc-Pep在不同Pep与Soc结合位点摩尔比例(1:1–32:1)下的偶联效率。使用Pep单独按10:1摩尔比例的反应作为对照(ctrl),证实Soc介导结合的特异性。 (e) gp23*和Soc-Pep条带灰度定量,并计算每个T4噬菌体展示的平均Pep拷贝数。 (f) Western blot分析证实Soc-Pep与PEDV阳性小鼠血清特异性结合(M:marker;1:T4;2:Soc-Pep)。

### 3.5 T4-Pep诱导强烈特异性抗体产生

为评估T4-Pep疫苗免疫原性,通过口服灌胃方式对小鼠免疫1.2 × 10¹² PFU T4-Pep噬菌体(相当于50 μg Pep)、50 μg游离Pep、T4以及PBS作为阴性对照(表2)。免疫程序遵循图5a所示方案。采集血清并通过ELISA定量PEDV特异性抗体滴度。与T4-Pep免疫小鼠相比,游离Pep免疫小鼠仅产生低水平PEDV特异性IgG;T4-Pep诱导了显著更强的抗体应答(图5b)。值得注意的是,T4-Pep制剂诱导高滴度特异性IgG抗体,峰值滴度达5 × 10⁴。第8周,采用固定病毒稀释法检测血清中和抗体滴度。与单独Pep组相比,T4-Pep免疫组对活PEDV表现出更高中和活性(图5c)。综合来看,这些发现表明T4噬菌体纳米颗粒平台具有强效免疫刺激作用。

**图5 小鼠中T4-Pep疫苗免疫原性评价。** (a) 免疫程序示意图。小鼠于第0、2、4和6周口服灌胃免疫,并于免疫后第2、4、6和8周采集血清。 (b) 免疫后第2、4、6和8周采集血清样品中PEDV特异性IgG抗体滴度,采用ELISA检测(n = 3,所有数据采用双尾t检验分析)。 (c) 第8周血清样品中和抗体滴度,采用固定病毒稀释法测定。免疫小鼠血清系列稀释后与PEDV孵育,中和滴度计算为显示完全中和的最高稀释度的倒数(n = 3,所有数据采用双尾t检验分析)。 (ns,无显著差异;* p < 0.05;** p < 0.01;*** p < 0.001)

### 3.6 T4-Pep对PEDV攻毒提供保护

完成加强免疫后,使用PEDV毒株CHN/SH-2012-5/2012感染小鼠,以探索T4-Pep的体内防御效果。随后连续7天监测其体重变化。如图6b所示,T4组和PBS组小鼠在病毒攻毒后出现进行性体重下降,而T4-Pep免疫小鼠在整个监测期内体重保持相对稳定。感染后第7天,采集肠道组织样品进行组织病理学评价。HE染色显示,与Pep、T4和PBS免疫组相比,T4-Pep免疫组小肠绒毛完整,无显著病理改变(图6a)。具体而言,T4组和PBS组显示明显绒毛萎缩和损伤(红色箭头,图6a、c),而单独Pep组显示轻度绒毛损伤和隐窝增生(黄色箭头,图6a、c)。肠道组织病毒载量分析显示,T4-Pep疫苗免疫小鼠组织中的病毒载量显著低于Pep疫苗免疫小鼠(图6d)。综合来看,这些结果表明T4噬菌体纳米颗粒平台在小鼠中对PEDV感染提供强效保护,有效减少病毒复制并维持肠道完整性。

**图6 Pep T4对小鼠PEDV攻毒的保护效力。** (a) 小鼠肠道组织代表性组织学图像(比例尺:200 μm)。病理改变包括绒毛损伤(红色箭头)和隐窝增生(黄色箭头)。 (b) PEDV感染后7天内小鼠每日体重变化(n = 6,所有数据采用双尾t检验分析)。 (c) 近端空肠绒毛长度测量(n = 6,所有数据采用双尾t检验分析)。 (d) 攻毒小鼠和对照小鼠近端空肠病毒载量,采用qRT-PCR定量(n = 3,所有数据采用双尾t检验分析)。 (ns,无显著差异;* p < 0.05;** p < 0.01;*** p < 0.001;**** p < 0.0001)

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## 4. 讨论

PEDV仍对全球养猪业构成严重威胁,给各年龄段猪群造成重大经济损失。在中国,近期猪群中报告了大规模腹泻暴发,PEDV被认为是50.90%病例的主要病毒病因,并在66.67%受影响猪场中被检测到。尽管目前已有抗PEDV商品化疫苗,但循环毒株的持续遗传进化削弱了其有效性,凸显了开发能够赋予广泛且持久保护的新型疫苗平台的迫切需求。

本研究设计了来源于PEDV S蛋白的多表位肽,并使用T4噬菌体纳米颗粒作为递送平台构建T4-Pep候选疫苗。该方法整合免疫信息学预测、结构生物学分析和纳米技术,以解决传统亚单位疫苗固有免疫原性低的局限,并评估口服免疫诱导免疫应答的潜力。

疫苗接种启动复杂免疫应答。在此过程中,B细胞通过抗体应答介导体液免疫,而CTL和HTL负责协调细胞免疫,这对清除病毒至关重要。因此,鉴定能够结合这些不同淋巴细胞群的病毒表位是理性疫苗设计的基础。免疫信息学方法已成为预测保护性抗原表位和加速疫苗开发的有力工具。

本研究以S蛋白作为疫苗表位筛选靶标。分析表明,第19–1326位氨基酸区域位于胞外结构域。对多个PEDV毒株S蛋白的进一步序列比对,包括高致病性G2c(AHCZO2)毒株,显示相似度超过91.46%,且鉴定所得线性表位在这些毒株中表现出高度保守性。这种显著保守性提示,基于这些表位的疫苗可能对多种PEDV变异株提供交叉保护,这是应对G2b和G2c等新兴毒株持续循环的关键特征。

本研究采用免疫信息学分析预测和筛选来源于PEDV S蛋白的免疫显性表位,并建立在已有表位预测框架之上。除表位选择外,有效疫苗设计还必须在增强免疫原性与可接受的反应原性和安全性之间取得平衡。为进一步评估疫苗-受体相互作用,本研究使用ClusPro服务器对多表位构建体(Pep)与TLR3进行分子对接。TLR3可识别PEDV复制过程中产生的双链RNA中间体,从而启动宿主固有免疫和干扰素应答。然而,PEDV感染细胞后,会利用多种病毒蛋白抑制TLR3信号通路并逃避免疫监视。因此,靶向TLR3是拮抗PEDV免疫逃逸并恢复宿主抗病毒防御的关键策略。分子对接可预测疫苗肽与TLR3的结合亲和力,从而在结构水平上验证所设计疫苗能否有效结合TLR3。此外,C-ImmSim模拟预测Pep构建体可诱导强烈体液和细胞免疫应答。

尽管基于表位的疫苗前景广阔,但肽类抗原免疫原性弱是其固有局限,需要高效递送平台以增强免疫激活。近年来,纳米生物技术的进展重新定义了病毒的角色:病毒不仅是病原体,也是具有多种生物医学应用的功能性纳米颗粒,包括疫苗递送。包括腺相关病毒(adeno-associated viruses, AAVs)和噬菌体在内的病毒结构蛋白已被成功工程化用于疫苗生产。在这些平台中,T4噬菌体作为疫苗递送系统最具前景。近年来,研究者广泛探索了多种新策略,如亚单位疫苗、病毒载体疫苗、核酸疫苗和黏膜递送系统,以克服传统疫苗在PEDV防控中的局限。然而,大多数新型疫苗仍面临免疫原性不足和抗原呈递效率有限等挑战。

与其他PEDV疫苗候选分子相比,T4-Pep平台表现出独特的免疫学优势。近期一项研究开发重组副干酪乳杆菌(*Lactobacillus paracasei*)生产抗PEDV亚单位疫苗候选分子。对妊娠小鼠口服免疫该重组菌株后,血清和肠道组织中PEDV特异性抗体滴度随时间逐渐升高。然而,尽管与对照组相比具有统计学显著升高,总体抗体水平仍相对有限。这些发现提示,仅S1蛋白免疫可能固有免疫原性有限,凸显了T4-Pep等多价展示平台在增强体液免疫应答方面的潜在优势。

结果显示,通过T4载体递送的等量Pep比单独Pep免疫诱导更高血清IgG水平。这些结果表明,本研究开发的T4噬菌体递送平台专门针对PEDV疫苗开发中的关键不足,在抗原呈递效率等方面表现出显著优势,为开发更契合PEDV感染特征、提供更稳定保护效果的新型疫苗提供了切实可行的技术路径。

尽管本研究开发的候选疫苗显示出巨大应用潜力,但仍有若干方面需要进一步研究。首先,本研究使用小鼠作为动物模型,而非自然宿主猪;因此,所诱导免疫应答特征和实际保护效力仍需在猪模型中进一步验证和评估。其次,本研究未直接检测黏膜相关指标,难以全面反映机体黏膜免疫状态。未来研究可纳入黏膜部位特异性检测指标,以更系统评价疫苗免疫原性。此外,由于该疫苗基于抗原表位而非全长抗原设计,其诱导的免疫谱与全抗原免疫存在一定差异,其潜在保护机制仍需进一步阐明。

总之,本研究利用T4噬菌体作为载体开发了一种PEDV疫苗平台,并进一步评估了其诱导免疫反应的能力。在小鼠模型中,T4-Pep对PEDV感染表现出显著保护效果,因此可作为PEDV预防的高度前景候选疫苗。

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**作者贡献** GuoQing Zhao:概念化、验证、方法学、撰写——初稿。 ShiDan Zhang:方法学、验证、撰写——审阅与编辑。 YuMin Zhang 和 ShengJing Jiao:验证。 XiaoYan Zeng:形式分析。 LuRu Zhao:方法学。 JingJiao Ma:调查研究。 YuQiang Cheng:可视化。 HengAn Wang:监督。 YaXian Yan 和 JianHe Sun:经费获取。 ZhaoFei Wang:项目管理、概念化。

**资助** 本研究由上海市科学技术委员会(资助号23N51900300)和国家自然科学基金(资助号32373097)资助。

**披露** 本研究所有参与者均已批准最终稿件。

**伦理声明** 涉及小鼠的实验程序严格遵循《实验动物饲养和使用指导原则》(中国),并经上海交通大学动物实验伦理委员会(中国)批准(批准号202201312)。

**利益冲突** 作者声明不存在利益冲突。