Porcine Anti-viral Immunity

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 14258

Special Issue Editor


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Guest Editor
College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou, China
Interests: veterinary vaccines; veterinary diagnostics; veterinary immunity

Special Issue Information

Dear Colleagues,

Innate and adaptive immunity protects pigs from viral infections. Understanding how porcine viruses interact with the host’s immune system is fundamental for the development of effective vaccines and anti-viral drugs. In this Special Issue, we will explore the mechanisms relating to how the porcine immune system fights against viral diseases and how viruses compromise and escape from the host immunity. 

For the above purpose, we welcome the submission of research articles, review articles, and short communications related to all aspects of interactions between porcine viruses and host immunity, porcine innate and adaptive immunity against viral infection, and the development of prophylactic and therapeutic vaccines against porcine diseases.

Prof. Dr. Kegong Tian
Guest Editor

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Keywords

  • Porcine viruses
  • Innate immunity
  • Adaptive immunity
  • Antiviral immunity

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Published Papers (6 papers)

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Research

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14 pages, 4178 KiB  
Article
Bergamottin Inhibits PRRSV Replication by Blocking Viral Non-Structural Proteins Expression and Viral RNA Synthesis
by Zhenbang Zhu, Yuqian Xu, Lulu Chen, Meng Zhang and Xiangdong Li
Viruses 2023, 15(6), 1367; https://doi.org/10.3390/v15061367 - 13 Jun 2023
Cited by 1 | Viewed by 1671
Abstract
The porcine reproductive and respiratory syndrome virus (PRRSV) causes economic losses in the swine industry worldwide. However, current vaccines cannot provide effective protection against PRRSV, and PRRSV-specific treatments for infected herds are still unavailable. In this study, we found that bergamottin showed strong [...] Read more.
The porcine reproductive and respiratory syndrome virus (PRRSV) causes economic losses in the swine industry worldwide. However, current vaccines cannot provide effective protection against PRRSV, and PRRSV-specific treatments for infected herds are still unavailable. In this study, we found that bergamottin showed strong inhibitory effects against PRRSV replication. Bergamottin inhibited PRRSV at the stage of the replication cycle. Mechanically, bergamottin promoted the activation of IRF3 and NF-κB signaling, leading to the increased expression of proinflammatory cytokines and interferon, which inhibited viral replication to some extent. In addition, bergamottion could reduce the expression of the non-structural proteins (Nsps), leading to the interruption of replication and transcription complex (RTC) formation and viral dsRNA synthesis, ultimately restraining PRRSV replication. Our study identified that bergamottin possesses potential value as an antiviral agent against PRRSV in vitro. Full article
(This article belongs to the Special Issue Porcine Anti-viral Immunity)
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16 pages, 5257 KiB  
Article
IFITM2 Presents Antiviral Response through Enhancing Type I IFN Signaling Pathway
by Lei Chen, Xiangrong Li, Yingying Deng, Yingjie Bi, Zhenfang Yan, Yanmei Yang, Xiangbo Zhang, Huixia Li, Jingying Xie and Ruofei Feng
Viruses 2023, 15(4), 866; https://doi.org/10.3390/v15040866 - 28 Mar 2023
Cited by 3 | Viewed by 1962
Abstract
Interferon (IFN) helps cells fight viral infections by further inducing the expression of many downstream IFN-stimulated genes (ISGs). Human interferon-inducible transmembrane proteins (IFITM) are one of these ISGs. The antiviral function of human IFITM1, IFITM2, and IFITM3 are well known. In this study, [...] Read more.
Interferon (IFN) helps cells fight viral infections by further inducing the expression of many downstream IFN-stimulated genes (ISGs). Human interferon-inducible transmembrane proteins (IFITM) are one of these ISGs. The antiviral function of human IFITM1, IFITM2, and IFITM3 are well known. In this study, we report that IFITM can significantly inhibit EMCV infectivity in HEK293 cells. Overexpression of IFITM proteins could promote IFN-β production. Meanwhile, IFITMs facilitated type I IFN signaling pathway adaptor MDA5 expression. We detected the binding of IFITM2 to MDA5 in a co-immunoprecipitation assay. It was also found that the ability of IFITM2 to activate IFN-β was significantly inhibited after interfering with MDA5 expression, suggesting that MDA5 may play an important role in the activation of the IFN-β signaling pathway by IFITM2. Moreover, the N-terminal domain plays an active role in the antiviral activity and the activation of IFN-β by IFITM2. These findings suggest that IFITM2 plays a vital role in antiviral signaling transduction. In addition, a positive feed-forward loop between IFITM2 and type I IFN establishes a key role for IFITM2 in enforcing innate immune responses. Full article
(This article belongs to the Special Issue Porcine Anti-viral Immunity)
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14 pages, 6011 KiB  
Article
Nonstructural Protein 2 Is Critical to Infection Efficiency of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus on PAMs and Influence Virulence In Vivo
by Jiazeng Chen, Lingxue Yu, Yanjun Zhou, Shen Yang, Yun Bai, Qian Wang, Jinmei Peng, Tongqing An, Fei Gao, Liwei Li, Chao Ye, Changlong Liu, Guangzhi Tong, Xuehui Cai, Zhijun Tian and Yifeng Jiang
Viruses 2022, 14(12), 2613; https://doi.org/10.3390/v14122613 - 23 Nov 2022
Cited by 2 | Viewed by 1639
Abstract
Porcine reproductive and respiratory syndrome (PRRS) is an important viral disease, causing significant economic losses to the swine industry worldwide. Atypical cases caused by highly pathogenic PRRS virus (HP-PRRSV) emerged in 2006 in China. The vaccine strain HuN4-F112 has been developed from the [...] Read more.
Porcine reproductive and respiratory syndrome (PRRS) is an important viral disease, causing significant economic losses to the swine industry worldwide. Atypical cases caused by highly pathogenic PRRS virus (HP-PRRSV) emerged in 2006 in China. The vaccine strain HuN4-F112 has been developed from the wild-type HP-PRRSV HuN4 through repeated passages on MARC-145 cells. However, the mechanisms of attenuation have yet to be defined. Previous studies have shown that the vaccine strain HuN4-F112 could not effectively replicate in porcine alveolar macrophages (PAMs). In the present study, a series of chimeric and mutant PRRSVs were constructed to investigate regions associated with the virus attenuation. Firstly, the corresponding genome regions (ORF1a, ORF1b and ORFs 2-7) were exchanged between two infectious clones of HuN4 and HuN4-F112, and then the influence of small regions in ORF1a and ORF2-7 was evaluated, then influence of specific amino acids on NSP2 was tested. NSP2 was determined to be the key gene that regulated infection efficiency on PAMs, and amino acids at 893 and 979 of NSP2 were the key amino acids. The results of in vivo study indicated that NSP2 was not only important for infection efficiency in vitro, but also influenced the virulence, which was indicated by the results of survival rate, temperature, viremia, lung score and tissue score. Full article
(This article belongs to the Special Issue Porcine Anti-viral Immunity)
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13 pages, 5267 KiB  
Article
IFIT3 and IFIT5 Play Potential Roles in Innate Immune Response of Porcine Pulmonary Microvascular Endothelial Cells to Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus
by Yanmei Wu, Xiaoxiao Song, Defeng Cui and Tao Zhang
Viruses 2022, 14(9), 1919; https://doi.org/10.3390/v14091919 - 30 Aug 2022
Cited by 7 | Viewed by 2120
Abstract
Our previous study has demonstrated that porcine pulmonary microvascular endothelial cells (MVECs) are susceptible to highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV). The innate immune response of MVECs infected with HP-PRRSV would play important roles in controlling virus proliferation, resisting cellular [...] Read more.
Our previous study has demonstrated that porcine pulmonary microvascular endothelial cells (MVECs) are susceptible to highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV). The innate immune response of MVECs infected with HP-PRRSV would play important roles in controlling virus proliferation, resisting cellular injury, and preventing the virus from spreading to other tissues and organs. Type I interferon is one of the most effective antiviral cytokines in the innate immune response, and interferon-induced proteins with tetratricopeptide repeats (IFITs) are members of interferon-stimulated genes induced by viruses and other pathogens, which are crucial in inhibiting virus proliferation and regulating the innate immune response. However, their effects on HP-PRRSV-induced innate immunity in porcine pulmonary MVECs remain unclear. Here, the roles of IFITs in porcine pulmonary MVECs infected with the HP-PRRSV HN strain were investigated, and the effects of astragalus polysaccharides (APS), a widely used traditional Chinese herbal ingredient with the immunopotentiating effect, on them were studied. The results showed that more autophagosomes were observed in HP-PRRSV-infected MVECs, and the expression of IFN-α, IFIT3, and IFIT5 decreased or increased at different time points after infection. When silencing the genes of IFIT3 or IFIT5, the HP-PRRSV replication in MVECs was significantly increased. The expression of IFIT3 and IFIT5 could be upregulated by APS, whose inhibitory effects on the HP-PRRSV replication significantly declined when the genes of IFIT3 or IFIT5 were silenced. The results suggest that IFIT3 and IFIT5 play an important role in inhibiting the HP-PRRSV replication in porcine pulmonary MVECs, and APS suppress the multiplication of HP-PRRSV by upregulating their expression. Full article
(This article belongs to the Special Issue Porcine Anti-viral Immunity)
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17 pages, 3891 KiB  
Article
Inducible miR-150 Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication by Targeting Viral Genome and Suppressor of Cytokine Signaling 1
by Sihan Li, Xuan Zhang, Yao Yao, Yingqi Zhu, Xiaojie Zheng, Fang Liu and Wenhai Feng
Viruses 2022, 14(7), 1485; https://doi.org/10.3390/v14071485 - 7 Jul 2022
Cited by 12 | Viewed by 2472
Abstract
Hosts exploit various approaches to defend against porcine reproductive and respiratory syndrome virus (PRRSV) infection. microRNAs (miRNAs) have emerged as key negative post-transcriptional regulators of gene expression and have been reported to play important roles in regulating virus infection. Here, we identified that [...] Read more.
Hosts exploit various approaches to defend against porcine reproductive and respiratory syndrome virus (PRRSV) infection. microRNAs (miRNAs) have emerged as key negative post-transcriptional regulators of gene expression and have been reported to play important roles in regulating virus infection. Here, we identified that miR-150 was differentially expressed in virus permissive and non-permissive cells. Subsequently, we demonstrated that PRRSV induced the expression of miR-150 via activating the protein kinase C (PKC)/c-Jun amino-terminal kinases (JNK)/c-Jun pathway, and overexpression of miR-150 suppressed PRRSV replication. Further analysis revealed that miR-150 not only directly targeted the PRRSV genome, but also facilitated type I IFN signaling. RNA immunoprecipitation assay demonstrated that miR-150 targeted the suppressor of cytokine signaling 1 (SOCS1), which is a negative regulator of Janus activated kinase (JAK)/signal transducer and activator of the transcription (STAT) signaling pathway. The inverse correlation between miR-150 and SOCS1 expression implies that miR-150 plays a role in regulating ISG expression. In conclusion, miR-150 expression is upregulated upon PRRSV infection. miR-150 feedback positively targets the PRRSV genome and promotes type I IFN signaling, which can be seen as a host defensive strategy. Full article
(This article belongs to the Special Issue Porcine Anti-viral Immunity)
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Review

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15 pages, 12033 KiB  
Review
Antagonisms of ASFV towards Host Defense Mechanisms: Knowledge Gaps in Viral Immune Evasion and Pathogenesis
by Liangzheng Yu, Zhenbang Zhu, Junhua Deng, Kegong Tian and Xiangdong Li
Viruses 2023, 15(2), 574; https://doi.org/10.3390/v15020574 - 19 Feb 2023
Cited by 7 | Viewed by 3474
Abstract
African swine fever (ASF) causes high morbidity and mortality of both domestic pigs and wild boars and severely impacts the swine industry worldwide. ASF virus (ASFV), the etiologic agent of ASF epidemics, mainly infects myeloid cells in swine mononuclear phagocyte system (MPS), including [...] Read more.
African swine fever (ASF) causes high morbidity and mortality of both domestic pigs and wild boars and severely impacts the swine industry worldwide. ASF virus (ASFV), the etiologic agent of ASF epidemics, mainly infects myeloid cells in swine mononuclear phagocyte system (MPS), including blood-circulating monocytes, tissue-resident macrophages, and dendritic cells (DCs). Since their significant roles in bridging host innate and adaptive immunity, these cells provide ASFV with favorable targets to manipulate and block their antiviral activities, leading to immune escape and immunosuppression. To date, vaccines are still being regarded as the most promising measure to prevent and control ASF outbreaks. However, ASF vaccine development is delayed and limited by existing knowledge gaps in viral immune evasion, pathogenesis, etc. Recent studies have revealed that ASFV can employ diverse strategies to interrupt the host defense mechanisms via abundant self-encoded proteins. Thus, this review mainly focuses on the antagonisms of ASFV-encoded proteins towards IFN-I production, IFN-induced antiviral response, NLRP3 inflammasome activation, and GSDMD-mediated pyroptosis. Additionally, we also make a brief discussion concerning the potential challenges in future development of ASF vaccine. Full article
(This article belongs to the Special Issue Porcine Anti-viral Immunity)
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