Special Issue "Animal Arteriviruses and Coronaviruses"
Quicklinks
A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".
Deadline for manuscript submissions: 30 June 2013
Special Issue Editor
Guest Editor
Dr. Xiuqing Wang
Department of Biology and Microbiology, Center for Infectious Disease Research and Vaccinology, South Dakota State University, SNP 252D, Box 2140D, Brookings, SD 57007, USA
Website: http://www.sdstate.edu/index/directory/directory-detail.cfm?view= detail&ci=2068
E-Mail: xiuqing.wang@sdstate.edu
Interests: arteriviruses; porcine reproductive and respiratory syndrome virus (PRRSV); coronaviruses; infectious bronchitis virus (IBV); viral immunity; viral pathogenesis; viral vectors; virus-cell interactions; moncyte-derived dendritic cells
Special Issue Information
Dear Colleagues,
Animal arteriviruses and coronaviruses, such as porcine reproductive and respiratory syndrome virus (PRRSV) and chicken infectious bronchitis virus (IBV), cause significant economic losses to the animal industry. PRRSV primarily infects macrophages and dendritic cells, which serve as an ideal model system to study host-pathogen interactions, especially the immune evasion mechanisms. Interestingly, IBV, a prototype of coronavirus, causes polyclonal activation of leukocytes in animals. Porcine respiratory coronavirus, on the other hand, has been used as a model system to better understand the pathogenesis of Severe Acute Respiratory Syndrome (SARS) virus in humans. Equine arteritis virus and bovine coronavirus are also important pathogens that cause severe diseases in their respective host species.
This special issue of “ Viruses” focuses on broad aspects of animal arteriviruses and coronaviruses, which include, but are not limited to, virus replication and assembly, virus-host interactions, role of viral structural and nonstructural proteins in viral pathogenesis and immunity, and their potential applications in vaccine development.
Dr. Xiuqing Wang
Guest Editor
Submission
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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a 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 1200 CHF (Swiss Francs).
Keywords
- arteriviruses
- coronaviruses
- replication and assembly
- pathogenesis
- innate immunity
- immune evasion
- vaccines
Published Papers (11 papers)
|
Received: 23 December 2011; in revised form: 10 January 2012 / Accepted: 14 January 2012 / Published: 18 January 2012
Show/Hide Abstract
| Download PDF Full-text (1556 KB) | Download XML Full-text | 
Abstract: Porcine reproductive and respiratory syndrome virus (PRRSV) can subvert early innate immunity, which leads to ineffective antimicrobial responses. Overcoming immune subversion is critical for developing vaccines and other measures to control this devastating swine virus. The overall goal of this work was to enhance innate and adaptive immunity following vaccination through the expression of interferon (IFN) genes by the PRRSV genome. We have constructed a series of recombinant PRRS viruses using an infectious PRRSV cDNA clone (pCMV-P129). Coding regions of exogenous genes, which included Renilla luciferase (Rluc), green and red fluorescent proteins (GFP and DsRed, respectively) and several interferons (IFNs), were constructed and expressed through a unique subgenomic mRNA placed between ORF1b and ORF2 of the PRRSV infectious clone. The constructs, which expressed Rluc, GFP, DsRed, efficiently produced progeny viruses and mimicked the parental virus in both MARC-145 cells and porcine macrophages. In contrast, replication of IFN-expressing viruses was attenuated, similar to the level of replication observed after the addition of exogenous IFN. Furthermore, the IFN expressing viruses inhibited the replication of a second PRRS virus co-transfected or co-infected. Inhibition by the different IFN subtypes corresponded to their anti-PRRSV activity, i.e., IFNω5 » IFNα1 > IFN-β > IFNδ3. In summary, the indicator-expressing viruses provided an efficient means for real-time monitoring of viral replication thus allowing high‑throughput elucidation of the role of host factors in PRRSV infection. This was shown when they were used to clearly demonstrate the involvement of tumor susceptibility gene 101 (TSG101) in the early stage of PRRSV infection. In addition, replication‑competent IFN-expressing viruses may be good candidates for development of modified live virus (MLV) vaccines, which are capable of reversing subverted innate immune responses and may induce more effective adaptive immunity against PRRSV infection.
|
|
Received: 24 December 2011; in revised form: 18 February 2012 / Accepted: 27 February 2012 / Published: 8 March 2012
Show/Hide Abstract
| Download PDF Full-text (839 KB) | Download XML Full-text
Abstract: The coronavirus E protein is a small membrane protein that has an important role in the assembly of virions. Recent studies have indicated that the E protein has functions during infection beyond assembly, including in virus egress and in the host stress response. Additionally, the E protein has ion channel activity, interacts with host proteins, and may have multiple membrane topologies. The goal of this review is to highlight the properties and functions of the E protein, and speculate on how they may be related.
|
|
Received: 5 January 2012; in revised form: 13 March 2012 / Accepted: 18 March 2012 / Published: 22 March 2012
Show/Hide Abstract
| Download PDF Full-text (1470 KB) | Download XML Full-text
Abstract: Equine arteritis virus (EAV) is a small, positive-stranded RNA virus. The glycoproteins gp2b, gp3 and gp4 form a heterotrimer in the viral envelope, which is required for cell entry of EAV. We describe expression of the ectodomains of the proteins in E. coli and their refolding from inclusion bodies. After extraction of inclusion bodies and dialysis, Gst-, but not His-tagged proteins, refold into a soluble conformation. However, when dialyzed together with Gst-gp3 or with Gst-gp4, His-gp2b and His-gp4 remain soluble and oligomers are obtained by affinity-chromatography. Thus, folding and oligomerization of gp2b, gp3 and gp4 in vitro are interdependent processes.
|
|
Received: 30 January 2012; in revised form: 15 March 2012 / Accepted: 18 March 2012 / Published: 2 April 2012
Show/Hide Abstract
| Download PDF Full-text (2045 KB) | Download XML Full-text
Abstract: Innate immunity is the first line of defense against viral infection, and in turn, viruses have evolved to evade host immune surveillance. As a result, viruses may persist in host and develop chronic infections. Type I interferons (IFN-α/β) are among the most potent antiviral cytokines triggered by viral infections. Porcine reproductive and respiratory syndrome (PRRS) is a disease of pigs that is characterized by negligible induction of type I IFNs and viral persistence for an extended period. For IFN production, RIG-I/MDA5 and JAK-STAT pathways are two major signaling pathways, and recent studies indicate that PRRS virus is armed to modulate type I IFN responses during infection. This review describes the viral strategies for modulation of type I IFN responses. At least three non‑structural proteins (Nsp1, Nsp2, and Nsp11) and a structural protein (N nucleocapsid protein) have been identified and characterized to play roles in the IFN suppression and NF-κB pathways. Nsp’s are early proteins while N is a late protein, suggesting that additional signaling pathways may be involved in addition to the IFN pathway. The understanding of molecular bases for virus-mediated modulation of host innate immune signaling will help us design new generation vaccines and control PRRS.
 |
|
Received: 20 March 2012; in revised form: 21 April 2012 / Accepted: 24 April 2012 / Published: 26 April 2012
Show/Hide Abstract
| Download PDF Full-text (302 KB) | Download XML Full-text
Abstract: Airborne transmission of porcine reproductive and respiratory syndrome virus (PRRSV) is a risk factor for the infection of susceptible populations. Therefore, a long‑term sustainability study of air filtration as a means to reduce this risk was conducted. Participating herds (n = 38) were organized into 4 independent cohorts and the effect of air filtration on the occurrence of new PRRSV infections was analyzed at 3 different levels from September 2008 to January 2012 including the likelihood of infection in contemporary filtered and non-filtered herds, the likelihood of infection before and after implementation of filtration and the time to failure in filtered and non-filtered herds. Results indicated that new PRRSV infections in filtered breeding herds were significantly lower than in contemporary non-filtered control herds (P < 0.01), the odds for a new PRRSV infection in breeding herds before filtration was 7.97 times higher than the odds after filtration was initiated (P < 0.01) and the median time to new PRRSV infections in filtered breeding herds of 30 months was significantly longer than the 11 months observed in non-filtered herds (P < 0.01). In conclusion, across all 3 levels of analysis, the long-term effect of air filtration on reducing the occurrence of new PRRSV infections in the study population was demonstrated.
 |
|
Received: 29 March 2012; in revised form: 18 April 2012 / Accepted: 24 April 2012 / Published: 2 May 2012
Show/Hide Abstract
| Download PDF Full-text (185 KB) | Download XML Full-text
Abstract: Porcine reproductive and respiratory syndrome virus (PRRSV) is not only a poor inducer of type I interferon but also inhibits the efficient induction of type I interferon by porcine transmissible gastroenteritis virus (TGEV) and synthetic dsRNA molecules, Poly I:C. However, the mechanistic basis by which PRRSV interferes with the induction of type I interferon in its natural host cells remains less well defined. The purposes of this review are to summarize the key findings in supporting the post-transcriptional control of type I interferon in its natural host cells and to propose the possible role of translational control in the regulation of type I interferon induction by PRRSV.
|
|
Received: 2 April 2012; in revised form: 3 May 2012 / Accepted: 7 May 2012 / Published: 15 May 2012
Show/Hide Abstract
| Download PDF Full-text (232 KB) | Download XML Full-text
Abstract: Regulatory T cells (Tregs) are a subset of T cells that are responsible for maintaining peripheral immune tolerance and homeostasis. The hallmark of Tregs is the expression of the forkhead box P3 (FoxP3) transcription factor. Natural regulatory T cells (nTregs) are a distinct population of T cells that express CD4 and FoxP3. nTregs develop in the thymus and function in maintaining peripheral immune tolerance. Other CD4+, CD4-CD8-, and CD8+CD28- T cells can be induced to acquire regulatory function by antigenic stimulation, depending on the cytokine milieu. Inducible (or adaptive) Tregs frequently express high levels of the interleukin 2 receptor (CD25). Atypical Tregs express FoxP3 and CD4 but have no surface expression of CD25. Type 1 regulatory T cells (Tr1 cells) produce IL-10, while T helper 3 cells (Th3) produce TGF-β. The function of inducible Tregs is presumably to maintain immune homeostasis, especially in the context of chronic inflammation or infection. Induction of Tregs in coronaviral infections protects against the more severe forms of the disease attributable to the host response. However, arteriviruses have exploited these T cell subsets as a means to dampen the immune response allowing for viral persistence. Treg induction or activation in the pathogenesis of disease has been described in both porcine reproductive and respiratory syndrome virus, lactate dehydrogenase elevating virus, and mouse hepatitis virus. This review discusses the development and biology of regulatory T cells in the context of arteriviral and coronaviral infection.
|
|
Received: 17 April 2012; in revised form: 12 May 2012 / Accepted: 23 May 2012 / Published: 24 May 2012
Show/Hide Abstract
| Download PDF Full-text (2888 KB) | Download XML Full-text
Abstract: Toll-like Receptors (TLRs) sense viral infections and induce production of type I interferons (IFNs), other cytokines, and chemokines. Viral recognition by TLRs and other pattern recognition receptors (PRRs) has been proven to be cell-type specific. Triggering of TLRs with selected ligands can be beneficial against some viral infections. Macrophages are antigen-presenting cells that express TLRs and have a key role in the innate and adaptive immunity against viruses. Coronaviruses (CoVs) are single-stranded, positive-sense RNA viruses that cause acute and chronic infections and can productively infect macrophages. Investigation of the interplay between CoVs and PRRs is in its infancy. We assessed the effect of triggering TLR2, TLR3, TLR4, and TLR7 with selected ligands on the susceptibility of the J774A.1 macrophage cell line to infection with murine coronavirus (mouse hepatitis virus, [MHV]). Stimulation of TLR2, TLR4, or TLR7 did not affect MHV production. In contrast, pre-stimulation of TLR3 with polyinosinic-polycytidylic acid (poly I:C) hindered MHV infection through induction of IFN-β in macrophages. We demonstrate that activation of TLR3 with the synthetic ligand poly I:C mediates antiviral immunity that diminishes (MHV-A59) or suppresses (MHV-JHM, MHV-3) virus production in macrophages.
|
|
Received: 7 May 2012; in revised form: 30 May 2012 / Accepted: 14 June 2012 / Published: 19 June 2012
Show/Hide Abstract
| Download PDF Full-text (890 KB) | Download XML Full-text
Abstract: Animal coronaviruses, such as infectious bronchitis virus (IBV), and arteriviruses, such as porcine reproductive and respiratory syndrome virus (PRRSV), are able to manifest highly contagious infections in their specific native hosts, thereby arising in critical economic damage to animal industries. This review discusses recent progress in studies of virus-host interactions during animal and human coronavirus and arterivirus infections, with emphasis on IBV-host cell interactions. These interactions may be directly involved in viral replication or lead to the alteration of certain signaling pathways, such as cell stress response and innate immunity, to facilitate viral replication and pathogenesis.
|
|
Received: 8 May 2012; in revised form: 13 June 2012 / Accepted: 14 June 2012 / Published: 20 June 2012
Show/Hide Abstract
| Download PDF Full-text (978 KB) | Download XML Full-text
Abstract: Coronaviruses are enveloped positive-stranded RNA viruses that replicate in the cytoplasm. To deliver their nucleocapsid into the host cell, they rely on the fusion of their envelope with the host cell membrane. The spike glycoprotein (S) mediates virus entry and is a primary determinant of cell tropism and pathogenesis. It is classified as a class I fusion protein, and is responsible for binding to the receptor on the host cell as well as mediating the fusion of host and viral membranes—A process driven by major conformational changes of the S protein. This review discusses coronavirus entry mechanisms focusing on the different triggers used by coronaviruses to initiate the conformational change of the S protein: receptor binding, low pH exposure and proteolytic activation. We also highlight commonalities between coronavirus S proteins and other class I viral fusion proteins, as well as distinctive features that confer distinct tropism, pathogenicity and host interspecies transmission characteristics to coronaviruses.
|
|
Received: 6 December 2012; in revised form: 14 January 2013 / Accepted: 15 January 2013 / Published: 18 January 2013
Show/Hide Abstract
| Download PDF Full-text (833 KB) | Download XML Full-text
Abstract: In previous studies, differences in the amount of genomic and subgenomic RNA produced by coronaviruses with mutations in the programmed ribosomal frameshift signal of ORF1a/b were observed. It was not clear if these differences were due to changes in genomic sequence, the protein sequence or the frequency of frameshifting. Here, viruses with synonymous codon changes are shown to produce different ratios of genomic and subgenomic RNA. These findings demonstrate that the protein sequence is not the primary cause of altered genomic and subgenomic RNA production. The synonymous codon changes affect both the structure of the frameshift signal and frameshifting efficiency. Small differences in frameshifting efficiency result in dramatic differences in genomic RNA production and TCID50 suggesting that the frameshifting frequency must stay above a certain threshold for optimal virus production. The data suggest that either the RNA sequence or the ratio of viral proteins resulting from different levels of frameshifting affects viral replication.
|
Last update: 17 April 2013
