Special Issue "Perspectives and Challenges in Coronavirus Research"
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A special issue of Viruses (ISSN 1999-4915).
Deadline for manuscript submissions: closed (31 January 2013)
Special Issue Editor
Guest Editor
Dr. Sonia Navas-Martin
Assistant Professor, Dept. of Microbiology & Immunology, Member, Center for Molecular Virology & Translational Neuroscience, Member, Institute for Molecular Medicine & Infectious Disease, Drexel University College of Medicine, 245 N. 15th Street, NCB Room 18309 MS1013A, Philadelphia, PA 19102 USA
Website: http://www.drexelmed.edu/Home/AboutOurFaculty/SoniaNavasMartin.aspx
E-Mail: Sonia.Navas-Martin@DrexelMed.edu
Phone: +215 762 7284
Fax: +215 762 8284
Special Issue Information
Dear Colleagues,
Coronaviruses (CoVs) are the most complex positive-sense single-stranded RNA (ssRNA+) viruses and cause acute self-limited and often fatal diseases in animals including humans. Since their discovery more than 50 years ago, some CoVs have been studied because of their veterinary relevance; other CoVs are considered useful models for human diseases such as neuroinflammation, multiple sclerosis, and hepatitis. Human CoVs are associated with mild respiratory tract disease and cause 30% of common cold in season. Just a decade ago a novel CoV was identified as the etiological agent of Severe Acute Respiratory Syndrome (SARS), the first pandemic of the 21st century. The identification of SARS-CoV has been a driver for the surge in CoV research in recent years. This special issue will contain reviews and original research papers on CoVs cross-species transmission, virus entry, replication and assembly, virus-host interactions, innate and adaptative immunity, pathogenesis, antivirals, vaccines and newly identified CoVs. We hope in this issue to capture the scope of these exciting developments and to provide perspectives and challenges in CoV research.
Dr. Sonia Navas-Martin
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
- coronaviruses
- SARS
- innate immunity
- pathogenesis
- virulence factor
- encephalitis
- chronic demyelination
- hepatitis
- lung
- cytokine storm
- antivirals
- vaccines
Published Papers (7 papers)
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Received: 23 August 2012; in revised form: 18 October 2012 / Accepted: 18 October 2012 / Published: 30 October 2012
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Abstract: The K-I and nephropathogenic K-II genotypes of infectious bronchitis virus (IBV) have been isolated since 1995 and 1990, respectively, in Korea and commercial inactivated oil-emulsion vaccines containing KM91 (K-II type) and Massachusetts 41 strains have been used in the field. To date, genomic analyses of Korean IBV strains and animal models to test the pathogenicity of Korean IBVs to the reproductive organs have been rare. In the present study, comparative genomics of SNU8067 (K-I type) and KM91 IBVs was performed, and an animal model to test the pathogenicity of SNU8067 was established and applied to vaccine efficacy test. The genome sizes of SNU8067 (27,708 nt) and KM91 (27,626 nt) were slightly different and the nucleotide and amino acid identities of the S1 (79%, 77%), 3a (65%, 52%), and 3b (81%, 72%) genes were lower than those of other genes (94%–97%, 92%–98%). A recombination analysis revealed that SNU8067 was a recombinant virus with a KM91-like backbone except S1, 3a, and 3b genes which might be from an unknown virus. An SNU8067 infection inhibited formation of hierarchal ovarian follicles (80%) and oviduct maturation (50%) in the control group, whereas 70% of vaccinated chickens were protected from lesions.
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Received: 1 October 2012; in revised form: 2 November 2012 / Accepted: 5 November 2012 / Published: 7 November 2012
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Abstract: A respiratory disease caused by a novel coronavirus, termed the severe acute respiratory syndrome coronavirus (SARS-CoV), was first reported in China in late 2002. The subsequent efficient human-to-human transmission of this virus eventually affected more than 30 countries worldwide, resulting in a mortality rate of ~10% of infected individuals. The spread of the virus was ultimately controlled by isolation of infected individuals and there has been no infections reported since April 2004. However, the natural reservoir of the virus was never identified and it is not known if this virus will re-emerge and, therefore, research on this virus continues. The SARS-CoV genome is about 30 kb in length and is predicted to contain 14 functional open reading frames (ORFs). The genome encodes for proteins that are homologous to known coronavirus proteins, such as the replicase proteins (ORFs 1a and 1b) and the four major structural proteins: nucleocapsid (N), spike (S), membrane (M) and envelope (E). SARS-CoV also encodes for eight unique proteins, called accessory proteins, with no known homologues. This review will summarize the current knowledge on SARS-CoV accessory proteins and will include: (i) expression and processing; (ii) the effects on cellular processes; and (iii) functional studies.
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Received: 5 October 2012; in revised form: 31 October 2012 / Accepted: 2 November 2012 / Published: 12 November 2012
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Abstract: The Coronaviridae family, an enveloped RNA virus family, and, more particularly, human coronaviruses (HCoV), were historically known to be responsible for a large portion of common colds and other upper respiratory tract infections. HCoV are now known to be involved in more serious respiratory diseases, i.e. bronchitis, bronchiolitis or pneumonia, especially in young children and neonates, elderly people and immunosuppressed patients. They have also been involved in nosocomial viral infections. In 2002–2003, the outbreak of severe acute respiratory syndrome (SARS), due to a newly discovered coronavirus, the SARS-associated coronavirus (SARS-CoV); led to a new awareness of the medical importance of the Coronaviridae family. This pathogen, responsible for an emerging disease in humans, with high risk of fatal outcome; underline the pressing need for new approaches to the management of the infection, and primarily to its prevention. Another interesting feature of coronaviruses is their potential environmental resistance, despite the accepted fragility of enveloped viruses. Indeed, several studies have described the ability of HCoVs (i.e. HCoV 229E, HCoV OC43 (also known as betacoronavirus 1), NL63, HKU1 or SARS-CoV) to survive in different environmental conditions (e.g. temperature and humidity), on different supports found in hospital settings such as aluminum, sterile sponges or latex surgical gloves or in biological fluids. Finally, taking into account the persisting lack of specific antiviral treatments (there is, in fact, no specific treatment available to fight coronaviruses infections), the Coronaviridae specificities (i.e. pathogenicity, potential environmental resistance) make them a challenging model for the development of efficient means of prevention, as an adapted antisepsis-disinfection, to prevent the environmental spread of such infective agents. This review will summarize current knowledge on the capacity of human coronaviruses to survive in the environment and the efficacy of well-known antiseptic-disinfectants against them, with particular focus on the development of new methodologies to evaluate the activity of new antiseptic-disinfectants on viruses.
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Brett E. Pickett, Douglas S. Greer, Yun Zhang, Lucy Stewart, Liwei Zhou, Guangyu Sun, Zhiping Gu, Sanjeev Kumar, Sam Zaremba, Christopher N. Larsen, Wei Jen, Edward B. Klem and Richard H. Scheuermann
Received: 2 October 2012; in revised form: 13 November 2012 / Accepted: 14 November 2012 / Published: 19 November 2012
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Abstract: Several viruses within the Coronaviridae family have been categorized as either emerging or re-emerging human pathogens, with Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) being the most well known. The NIAID-sponsored Virus Pathogen Database and Analysis Resource (ViPR, www.viprbrc.org) supports bioinformatics workflows for a broad range of human virus pathogens and other related viruses, including the entire Coronaviridae family. ViPR provides access to sequence records, gene and protein annotations, immune epitopes, 3D structures, host factor data, and other data types through an intuitive web-based search interface. Records returned from these queries can then be subjected to web-based analyses including: multiple sequence alignment, phylogenetic inference, sequence variation determination, BLAST comparison, and metadata-driven comparative genomics statistical analysis. Additional tools exist to display multiple sequence alignments, view phylogenetic trees, visualize 3D protein structures, transfer existing reference genome annotations to new genomes, and store or share results from any search or analysis within personal private ‘Workbench’ spaces for future access. All of the data and integrated analysis and visualization tools in ViPR are made available without charge as a service to the Coronaviridae research community to facilitate the research and development of diagnostics, prophylactics, vaccines and therapeutics against these human pathogens.
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Received: 21 October 2012; in revised form: 14 November 2012 / Accepted: 15 November 2012 / Published: 21 November 2012
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Abstract: Coronaviruses are positive-strand RNA viruses that are important infectious agents of both animals and humans. A common feature among positive-strand RNA viruses is their assembly of replication-transcription complexes in association with cytoplasmic membranes. Upon infection, coronaviruses extensively rearrange cellular membranes into organelle-like replicative structures that consist of double-membrane vesicles and convoluted membranes to which the nonstructural proteins involved in RNA synthesis localize. Double-stranded RNA, presumably functioning as replicative intermediate during viral RNA synthesis, has been detected at the double-membrane vesicle interior. Recent studies have provided new insights into the assembly and functioning of the coronavirus replicative structures. This review will summarize the current knowledge on the biogenesis of the replicative structures, the membrane anchoring of the replication-transcription complexes, and the location of viral RNA synthesis, with particular focus on the dynamics of the coronavirus replicative structures and individual replication-associated proteins.
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Received: 27 September 2012; in revised form: 26 November 2012 / Accepted: 27 November 2012 / Published: 30 November 2012
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Abstract: Coronaviruses are single stranded, positive sense RNA viruses, which induce the rearrangement of cellular membranes upon infection of a host cell. This provides the virus with a platform for the assembly of viral replication complexes, improving efficiency of RNA synthesis. The membranes observed in coronavirus infected cells include double membrane vesicles. By nature of their double membrane, these vesicles resemble cellular autophagosomes, generated during the cellular autophagy pathway. In addition, coronavirus infection has been demonstrated to induce autophagy. Here we review current knowledge of coronavirus induced membrane rearrangements and the involvement of autophagy or autophagy protein microtubule associated protein 1B light chain 3 (LC3) in coronavirus replication.
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Received: 11 October 2012; in revised form: 13 November 2012 / Accepted: 23 November 2012 / Published: 12 December 2012
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Abstract: In 2007, a novel coronavirus associated with an acute respiratory disease in alpacas (Alpaca Coronavirus, ACoV) was isolated. Full-length genomic sequencing of the ACoV demonstrated the genome to be consistent with other Alphacoronaviruses. A putative additional open-reading frame was identified between the nucleocapsid gene and 3'UTR. The ACoV was genetically most similar to the common human coronavirus (HCoV) 229E with 92.2% nucleotide identity over the entire genome. A comparison of spike gene sequences from ACoV and from HCoV-229E isolates recovered over a span of five decades showed the ACoV to be most similar to viruses isolated in the 1960’s to early 1980’s. The true origin of the ACoV is unknown, however a common ancestor between the ACoV and HCoV-229E appears to have existed prior to the 1960’s, suggesting virus transmission, either as a zoonosis or anthroponosis, has occurred between alpacas and humans.
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Planned Papers
The below list represents only planned manuscripts. Some of these
manuscripts have not been received by the Editorial Office yet. Papers
submitted to MDPI journals are subject to peer-review.
Type of Paper: Review
Title: Innate Immune evasion of murine Coronaviruses and SARS-CoV and its Implications in Pathogenesis
Authors: Sonia Navas-Martin 1,2* and Renzo Perales-Linares1,2
Affiliation: 1Department of Microbiology and Immunology, 2 Center for Molecular Virology and Translational Neuroscience, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA 19102, USA
E-Mails: sonia.navas-martin@drexelmed.edu (S.N.M.); rfp35@drexel.edu (R.P.L.)
* Author to whom correspondence should be addressed; Tel: +1 215 762 7284, Fax: + 1 215 762 8284,sonia.navas-martin@drexelmed.edu
Abstract: How coronaviruses are sensed by the innate immune response, and in particular, by pattern recognition receptors (PRRs) remains poorly characterized. Recently, a few PRRs that sense murine coronaviruses and Severe Acute Respiratory Syndrome CoV (SARS) in a cell-type dependent manner have been identified, although its role in pathogenesis remains to be defined. In addition, emerging evidence suggest that coronaviruses have evolved evasion and countermeasures mechanisms to antagonize the innate immune response. Here we review our current understanding of the molecular mechanisms of coronavirus evasion and counteraction of the innate immune response, and discuss its implications in pathogenesis focusing in murine coronaviruses and SARS.
Keywords: coronavirus, viral countermeasure, SARS, pattern recognition receptors, innate immune evasion, IFN, TLR
Last update: 28 January 2013