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Special Issue "Porcine Viruses 2019"

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

Deadline for manuscript submissions: 31 May 2019

Special Issue Editors

Guest Editor
Dr. Elisa Crisci

Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, NC, USA
Website | E-Mail
Interests: porcine viruses; virus–innate immunity interaction; swine influenza; PRRSV
Guest Editor
Dr. Maria Montoya

Centro de Investigaciones Biológicas (CIB), CSIC, Madrid, Spain
Website | E-Mail
Interests: porcine viruses; swine influenza virus; virus–host interaction; African swine fever virus

Special Issue Information

Dear Colleagues,

We are honored to have this opportunity to guest-edit a Special Issue on porcine viruses.

The global pig industry is facing major new and old challenges caused by emerging and re-emerging viral infections. One of the more recent is the emergence of African swine fever virus (ASFV) in several countries of Eastern Europe and Asia. In the same way, classical swine fever (CSFV) is re-emerging in Japan and Brazil.

Concomitant to those new outbreaks, swine production is still struggling with porcine reproductive and respiratory syndrome virus (PRRSV) as well as porcine epidemic diarrhea virus (PEDV) endemics due to the lack of an effective vaccination system. Additionally, porcine deltacoronavirus (PDCoV) detection is increasing in the US and Asia. Other viruses such swine influenza virus (SwIV) or foot-and-mouth disease virus (FMDV) still pose a threat to pig health.

In light of the contribution of pig production to food security, new measures and basic knowledge are required when attempting to control the spread of such devastating epidemic viruses and to reduce the incidence of the endemic ones.

In this Special Issue, we will outline the new discoveries in relevant porcine viruses, knowledge gaps, and how this information will help to cope with the future challenges for the global swine industry. We invite porcine virologists worldwide to tell their most exciting stories in the form of original research articles or opinion/hypothesis essays. Focus on the molecular biology of the virus, virus–host interactions, and the development of new therapies is highly appreciated.

Dr. Elisa Crisci
Dr. Maria Montoya
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • viruses
  • pig
  • host–pathogen interaction
  • vaccine

Published Papers (10 papers)

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Research

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Open AccessArticle
Characteristics of the Life Cycle of Porcine Deltacoronavirus (PDCoV) In Vitro: Replication Kinetics, Cellular Ultrastructure and Virion Morphology, and Evidence of Inducing Autophagy
Viruses 2019, 11(5), 455; https://doi.org/10.3390/v11050455
Received: 10 April 2019 / Revised: 15 May 2019 / Accepted: 16 May 2019 / Published: 18 May 2019
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Abstract
Porcine deltacoronavirus (PDCoV) causes severe diarrhea and vomiting in affected piglets. The aim of this study was to establish the basic, in vitro characteristics of the life cycle such as replication kinetics, cellular ultrastructure, virion morphology, and induction of autophagy of PDCoV. Time-course [...] Read more.
Porcine deltacoronavirus (PDCoV) causes severe diarrhea and vomiting in affected piglets. The aim of this study was to establish the basic, in vitro characteristics of the life cycle such as replication kinetics, cellular ultrastructure, virion morphology, and induction of autophagy of PDCoV. Time-course analysis of viral subgenomic and genomic RNA loads and infectious titers indicated that one replication cycle of PDCoV takes 5 to 6 h. Electron microscopy showed that PDCoV infection induced the membrane rearrangements with double-membrane vesicles and large virion-containing vacuoles. The convoluted membranes structures described in alpha- and beta-coronavirus were not observed. PDCoV infection also increased the number of autophagosome-like vesicles in the cytoplasm of cells, and the autophagy response was detected by LC3 I/II and p62 Western blot analysis. For the first time, this study presents the picture of the PDCoV infection cycle, which is crucial to help elucidate the molecular mechanism of deltacoronavirus replication. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Open AccessArticle
Porcine Parvovirus Infection Causes Pig Placenta Tissue Damage Involving Nonstructural Protein 1 (NS1)-Induced Intrinsic ROS/Mitochondria-Mediated Apoptosis
Viruses 2019, 11(4), 389; https://doi.org/10.3390/v11040389
Received: 28 February 2019 / Revised: 21 April 2019 / Accepted: 23 April 2019 / Published: 25 April 2019
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Abstract
Porcine parvovirus (PPV) is an important pathogen causing reproductive failure in pigs. PPV-induced cell apoptosis has been recently identified as being involved in PPV-induced placental tissue damages resulting in reproductive failure. However, the molecular mechanism was not fully elucidated. Here we demonstrate that [...] Read more.
Porcine parvovirus (PPV) is an important pathogen causing reproductive failure in pigs. PPV-induced cell apoptosis has been recently identified as being involved in PPV-induced placental tissue damages resulting in reproductive failure. However, the molecular mechanism was not fully elucidated. Here we demonstrate that PPV nonstructural protein 1 (NS1) can induce host cell apoptosis and death, thereby indicating the NS1 may play a crucial role in PPV-induced placental tissue damages and reproductive failure. We have found that NS1-induced apoptosis was significantly inhibited by caspase 9 inhibitor, but not caspase 8 inhibitor, and transfection of NS1 gene into PK-15 cells significantly inhibited mitochondria-associated antiapoptotic molecules Bcl-2 and Mcl-1 expressions and enhanced proapoptotic molecules Bax, P21, and P53 expressions, suggesting that NS1-induced apoptosis is mainly through the mitochondria-mediated intrinsic apoptosis pathway. We also found that both PPV infection and NS1 vector transfection could cause host DNA damage resulting in cell cycle arrest at the G1 and G2 phases, trigger mitochondrial ROS accumulation resulting in mitochondria damage, and therefore, induce the host cell apoptosis. This study provides a molecular basis for elucidating PPV-induced cell apoptosis and reproductive failure. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Open AccessArticle
Porcine Epidemic Diarrhea Virus (PEDV) ORF3 Interactome Reveals Inhibition of Virus Replication by Cellular VPS36 Protein
Viruses 2019, 11(4), 382; https://doi.org/10.3390/v11040382
Received: 26 March 2019 / Revised: 19 April 2019 / Accepted: 23 April 2019 / Published: 24 April 2019
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Abstract
The accessory protein ORF3 of porcine epidemic diarrhea virus (PEDV) has been proposed to play a key role in virus replication. However, our understanding of its function regarding virus and host interaction is still limited. In this study, we employed immunoprecipitation and mass [...] Read more.
The accessory protein ORF3 of porcine epidemic diarrhea virus (PEDV) has been proposed to play a key role in virus replication. However, our understanding of its function regarding virus and host interaction is still limited. In this study, we employed immunoprecipitation and mass spectrometry to screen for cellular interacting partners of ORF3. Gene ontology analysis of the host interactome highlighted the involvement of ORF3 in endosomal and immune signaling pathways. Among the identified ORF3-interacting proteins, the vacuolar protein-sorting-associated protein 36 (VPS36) was assessed for its role in PEDV replication. VPS36 was found to interact with ORF3 regardless of its GLUE domain. As a result of VPS36–ORF3 interaction, PEDV replication was substantially suppressed in cells overexpressing VPS36. Interestingly, the ORF3 protein expression was diminished in VPS36-overexpressing cells, an effect that could not be restored by treatment of lysosomal inhibitors. In addition, disruption of endogenously-expressed VPS36 by siRNA could partially augment PEDV replication. Taken together, our study provides mechanistic insights into the contribution of ORF3 in PEDV replication. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Open AccessArticle
The N-Terminal Domain of Spike Protein Is Not the Enteric Tropism Determinant for Transmissible Gastroenteritis Virus in Piglets
Viruses 2019, 11(4), 313; https://doi.org/10.3390/v11040313
Received: 4 March 2019 / Revised: 24 March 2019 / Accepted: 26 March 2019 / Published: 30 March 2019
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Abstract
Transmissible gastroenteritis virus (TGEV) is the etiologic agent of transmissible gastroenteritis in pigs, and the N-terminal domain of TGEV spike protein is generally recognized as both the virulence determinant and enteric tropism determinant. Here, we assembled a full-length infectious cDNA clone of TGEV [...] Read more.
Transmissible gastroenteritis virus (TGEV) is the etiologic agent of transmissible gastroenteritis in pigs, and the N-terminal domain of TGEV spike protein is generally recognized as both the virulence determinant and enteric tropism determinant. Here, we assembled a full-length infectious cDNA clone of TGEV in a bacterial artificial chromosome. Using a novel approach, the clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9) systems efficiently and rapidly rescued another recombinant virus with a 224-amino-acid deletion in the N-terminal domain of the TGEV Spike gene (S_NTD224), which is analogous to the N-terminal domain of porcine respiratory coronavirus. S_NTD224 notably affected the TGEV growth kinetics in PK-15 cells but was not essential for recombinant virus survival. In animal experiments with 13 two-day-old piglets, the TGEV recombinant viruses with/without S_NTD224 deletion induced obvious clinical signs and mortality. Together, our results directly demonstrated that S_NTD224 of TGEV mildly influenced TGEV virulence but was not the enteric tropism determinant and provide new insights for the development of a new attenuated vaccine against TGEV. Importantly, the optimized reverse genetics platform used in this study will simplify the construction of mutant infectious clones and help accelerate progress in coronavirus research. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Open AccessArticle
Interaction of Structural Glycoprotein E2 of Classical Swine Fever Virus with Protein Phosphatase 1 Catalytic Subunit Beta (PPP1CB)
Viruses 2019, 11(4), 307; https://doi.org/10.3390/v11040307
Received: 27 February 2019 / Revised: 22 March 2019 / Accepted: 25 March 2019 / Published: 29 March 2019
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Abstract
Classical swine fever virus (CSFV) E2 protein, the major virus structural glycoprotein, is an essential component of the viral envelope. E2 is involved in virus absorption, induction of a protective immune response and is critical for virulence in swine. Using the yeast two-hybrid [...] Read more.
Classical swine fever virus (CSFV) E2 protein, the major virus structural glycoprotein, is an essential component of the viral envelope. E2 is involved in virus absorption, induction of a protective immune response and is critical for virulence in swine. Using the yeast two-hybrid system, we identified protein phosphatase 1 catalytic subunit beta (PPP1CB), which is part of the Protein Phosphatase 1 (PP1) complex, as a specific binding host partner for E2. We further confirmed the occurrence of this interaction in CSFV-infected swine cells by using two independent methodologies: Co-immunoprecipitation and Proximity Ligation Assay. In addition, we demonstrated that pharmacological activation of the PP1 pathway has a negative effect on CSFV replication while inhibition of the PP1 pathway or knockdown of PPP1CB by siRNA had no observed effect. Overall, our data suggests that the CSFV E2 and PPP1CB protein interact in infected cells, and that activation of the PP1 pathway decreases virus replication. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Open AccessArticle
A Field Recombinant Strain Derived from Two Type 1 Porcine Reproductive and Respiratory Syndrome Virus (PRRSV-1) Modified Live Vaccines Shows Increased Viremia and Transmission in SPF Pigs
Viruses 2019, 11(3), 296; https://doi.org/10.3390/v11030296
Received: 28 January 2019 / Revised: 15 March 2019 / Accepted: 21 March 2019 / Published: 23 March 2019
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Abstract
In Europe, modified live vaccines (MLV) are commonly used to control porcine reproductive and respiratory syndrome virus (PRRSV) infection. However, they have been associated with safety issues such as reversion to virulence induced by mutation and/or recombination. On a French pig farm, we [...] Read more.
In Europe, modified live vaccines (MLV) are commonly used to control porcine reproductive and respiratory syndrome virus (PRRSV) infection. However, they have been associated with safety issues such as reversion to virulence induced by mutation and/or recombination. On a French pig farm, we identified a field recombinant strain derived from two PRRSV-1 MLV (MLV1). As a result, we aimed to evaluate its clinical, virological, and transmission parameters in comparison with both parental strains. Three groups with six pigs in each were inoculated with either one of the two MLV1s or with the recombinant strain; six contact pigs were then added into each inoculated group. The animals were monitored daily for 35 days post-inoculation (dpi) for clinical symptoms; blood samples and nasal swabs were collected twice a week. PRRS viral load in inoculated pigs of recombinant group was higher in serum, nasal swabs, and tonsils in comparison with both vaccine groups. The first viremic contact pig was detected as soon as 2 dpi in the recombinant group compared to 10 and 17 dpi for vaccine groups. Estimation of transmission parameters revealed fastest transmission and longest duration of infectiousness for recombinant group. Our in vivo study showed that the field recombinant strain derived from two MLV1s demonstrated high viremia, shedding and transmission capacities. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Open AccessArticle
A Single V672F Substitution in the Spike Protein of Field-Isolated PEDV Promotes Cell–Cell Fusion and Replication in VeroE6 Cells
Viruses 2019, 11(3), 282; https://doi.org/10.3390/v11030282
Received: 6 February 2019 / Revised: 15 March 2019 / Accepted: 19 March 2019 / Published: 20 March 2019
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Abstract
While porcine epidemic diarrhea virus (PEDV) infects and replicates in enterocytes lining villi of neonatal piglets with high efficiency, naturally isolated variants typically grow poorly in established cell lines, unless adapted by multiple passages. Cells infected with most cell-adapted PEDVs usually displayed large [...] Read more.
While porcine epidemic diarrhea virus (PEDV) infects and replicates in enterocytes lining villi of neonatal piglets with high efficiency, naturally isolated variants typically grow poorly in established cell lines, unless adapted by multiple passages. Cells infected with most cell-adapted PEDVs usually displayed large syncytia, a process triggered by the spike protein (S). To identify amino acids responsible for S-mediated syncytium formation, we constructed and characterized chimeric S proteins of the cell-adapted variant, YN144, in which the receptor binding domain (RBD) and S1/S2 cleavage site were replaced with those of a poorly culturable field isolate (G2). We demonstrated that the RBD, not the S1/S2 cleavage site, is critical for syncytium formation mediated by chimeric S proteins. Further mutational analyses revealed that a single mutation at the amino acid residue position 672 (V672F) could enable the chimeric S with the entire RBD derived from the G2 strain to trigger large syncytia. Moreover, recombinant PEDV viruses bearing S of the G2 strain with the single V672F substitution could induce extensive syncytium formation and replicate efficiently in VeroE6 cells stably expressing porcine aminopeptidase N (VeroE6-APN). Interestingly, we also demonstrated that while the V672F mutation is critical for the syncytium formation in VeroE6-APN cells, it exerts a minimal effect in Huh-7 cells, thereby suggesting the difference in receptor preference of PEDV among host cells. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Open AccessArticle
Retrospective Detection and Genetic Characterization of Porcine circovirus 3 (PCV3) Strains Identified between 2006 and 2007 in Brazil
Viruses 2019, 11(3), 201; https://doi.org/10.3390/v11030201
Received: 22 January 2019 / Revised: 15 February 2019 / Accepted: 22 February 2019 / Published: 27 February 2019
Cited by 1 | PDF Full-text (1226 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Porcine circovirus 3 (PCV3) is an emerging virus that was first identified in the United States in 2016. Since its first detection, PCV3 has already been found in America, Asia, and Europe. Although PCV3 has already been described in Brazil, knowledge of its [...] Read more.
Porcine circovirus 3 (PCV3) is an emerging virus that was first identified in the United States in 2016. Since its first detection, PCV3 has already been found in America, Asia, and Europe. Although PCV3 has already been described in Brazil, knowledge of its detection and sequence variation before 2016 is limited, as well as its distribution in the main swine producing regions of Brazil. In this study, 67 porcine clinical samples collected from nine states in Brazil between 2006 and 2007 were analyzed for PCV3 infection by PCR. Results showed that 47.8% of the samples were PCV3 positive, across all nine states. Of the PCV3-positive samples, 37.5% were also positive for PCV2. Interestingly, no clinical signs were associated with samples that were detected singularly with PCV3 infection. Moreover, the positive PCV3 rate in healthy pigs was higher (29.8%) than that found in unhealthy pigs (17.9%), suggesting that most pigs could live with PCV3 infection without any clinical sign in the analyzed samples. Nucleotide sequence analysis showed that PCV3 strains obtained in this study shared 94.44% to 99.83% sequence identity at the open reading frame 2 (ORF2) gene level with available strains from different countries. PCV3 Brazilian sequences collected in 2006 and 2007 shared 97.94% to 99.62% identity with the strains obtained in 2016. The results of neutrality and selective pressure tests indicated that the PCV3 Cap protein seems unable to tolerate high levels of variation on its sequence. Phylogenetic analysis grouped the Brazilian strains in PCV3a and PCV3b genotypes clusters, both including strains collected in America, Asia, and Europe. Taking the results together, multiple events of introduction of PCV3 may have occurred in Brazil, and Brazilian PCV3 strains may show genetic stability over the past 10 years. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Review

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Open AccessReview
Porcine Dendritic Cells and Viruses: An Update
Viruses 2019, 11(5), 445; https://doi.org/10.3390/v11050445
Received: 29 April 2019 / Revised: 12 May 2019 / Accepted: 14 May 2019 / Published: 16 May 2019
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Abstract
Several viral infections of swine are responsible for major economic losses and represent a threat to the swine industry worldwide. New tools are needed to prevent and control endemic, emerging, and re-emerging viral diseases. Dendritic cells (DC) play a central role in linking [...] Read more.
Several viral infections of swine are responsible for major economic losses and represent a threat to the swine industry worldwide. New tools are needed to prevent and control endemic, emerging, and re-emerging viral diseases. Dendritic cells (DC) play a central role in linking the innate and adaptive arms of the immune system, so knowledge regarding their interaction with pathogens is necessary to understand the mechanisms underlying diseases pathogenesis and protection. In the first part of this review, we provide an update on the heterogeneous cell subsets that comprise the porcine DC family. In the second part of this review, we provide an overview of how three viruses, affecting pork production at a global level, African swine fever virus (ASFV), classical swine fever virus (CSFV), and porcine circovirus 2 (PCV2), modulate DC function. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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Open AccessReview
Co-Infection of Swine with Porcine Circovirus Type 2 and Other Swine Viruses
Viruses 2019, 11(2), 185; https://doi.org/10.3390/v11020185
Received: 6 January 2019 / Revised: 18 February 2019 / Accepted: 21 February 2019 / Published: 21 February 2019
Cited by 1 | PDF Full-text (243 KB) | HTML Full-text | XML Full-text
Abstract
Porcine circovirus 2 (PCV2) is the etiological agent that causes porcine circovirus diseases and porcine circovirus-associated diseases (PCVD/PCVAD), which are present in every major swine-producing country in the world. PCV2 infections may downregulate the host immune system and enhance the infection and replication [...] Read more.
Porcine circovirus 2 (PCV2) is the etiological agent that causes porcine circovirus diseases and porcine circovirus-associated diseases (PCVD/PCVAD), which are present in every major swine-producing country in the world. PCV2 infections may downregulate the host immune system and enhance the infection and replication of other pathogens. However, the exact mechanisms of PCVD/PCVAD are currently unknown. To date, many studies have reported that several cofactors, such as other swine viruses or bacteria, vaccination failure, and stress or crowding, in combination with PCV2, lead to PCVD/PCVAD. Among these cofactors, co-infection of PCV2 with other viruses, such as porcine reproductive and respiratory syndrome virus, porcine parvovirus, swine influenza virus and classical swine fever virus have been widely studied for decades. In this review, we focus on the current state of knowledge regarding swine co-infection with different PCV2 genotypes or strains, as well as with PCV2 and other swine viruses. Full article
(This article belongs to the Special Issue Porcine Viruses 2019)
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