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      Middle East respiratory syndrome coronavirus: transmission, virology and therapeutic targeting to aid in outbreak control

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          Abstract

          Middle East respiratory syndrome coronavirus (MERS-CoV) causes high fever, cough, acute respiratory tract infection and multiorgan dysfunction that may eventually lead to the death of the infected individuals. MERS-CoV is thought to be transmitted to humans through dromedary camels. The occurrence of the virus was first reported in the Middle East and it subsequently spread to several parts of the world. Since 2012, about 1368 infections, including ~487 deaths, have been reported worldwide. Notably, the recent human-to-human ‘superspreading' of MERS-CoV in hospitals in South Korea has raised a major global health concern. The fatality rate in MERS-CoV infection is four times higher compared with that of the closely related severe acute respiratory syndrome coronavirus infection. Currently, no drug has been clinically approved to control MERS-CoV infection. In this study, we highlight the potential drug targets that can be used to develop anti-MERS-CoV therapeutics.

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          Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia.

          Theo M. Bestebroer, Albert Osterhaus, Sander van Boheemen … (2012)
          A previously unknown coronavirus was isolated from the sputum of a 60-year-old man who presented with acute pneumonia and subsequent renal failure with a fatal outcome in Saudi Arabia. The virus (called HCoV-EMC) replicated readily in cell culture, producing cytopathic effects of rounding, detachment, and syncytium formation. The virus represents a novel betacoronavirus species. The closest known relatives are bat coronaviruses HKU4 and HKU5. Here, the clinical data, virus isolation, and molecular identification are presented. The clinical picture was remarkably similar to that of the severe acute respiratory syndrome (SARS) outbreak in 2003 and reminds us that animal coronaviruses can cause severe disease in humans.
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            Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus

            Wenhui Li, Michael Moore, Natalya Vasilieva … (2003)
            Spike (S) proteins of coronaviruses, including the coronavirus that causes severe acute respiratory syndrome (SARS), associate with cellular receptors to mediate infection of their target cells 1,2 . Here we identify a metallopeptidase, angiotensin-converting enzyme 2 (ACE2) 3,4 , isolated from SARS coronavirus (SARS-CoV)-permissive Vero E6 cells, that efficiently binds the S1 domain of the SARS-CoV S protein. We found that a soluble form of ACE2, but not of the related enzyme ACE1, blocked association of the S1 domain with Vero E6 cells. 293T cells transfected with ACE2, but not those transfected with human immunodeficiency virus-1 receptors, formed multinucleated syncytia with cells expressing S protein. Furthermore, SARS-CoV replicated efficiently on ACE2-transfected but not mock-transfected 293T cells. Finally, anti-ACE2 but not anti-ACE1 antibody blocked viral replication on Vero E6 cells. Together our data indicate that ACE2 is a functional receptor for SARS-CoV. Supplementary information The online version of this article (doi:10.1038/nature02145) contains supplementary material, which is available to authorized users.
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              The spike protein of SARS-CoV — a target for vaccine and therapeutic development

              Lanying Du, Yuxian He, Yusen Zhou … (2009)
              Key Points This Review provides an overview on the spike (S) protein of severe acute respiratory syndrome-coronavirus (SARS-CoV) as a target for the development of vaccines and therapeutics for the prevention and treatment of SARS. SARS is a newly emerging infectious disease, caused by SARS-CoV, a novel coronavirus that caused a global outbreak of SARS. SARS-CoV S protein mediates binding of the virus with its receptor angiotensin-converting enzyme 2 and promotes the fusion between the viral and host cell membranes and virus entry into the host cell. SARS-CoV S protein induces humoral and cellular immune responses against SARS-CoV. SARS S protein is the target of new SARS vaccines. These vaccines are based on SARS-CoV full-length S protein and its receptor-binding domain, including DNA-, viral vector- and subunit-based vaccines Peptides, antibodies, organic compounds and short interfering RNAs are additional anti-SARS-CoV therapeutics that target the S protein. The work on SARS-CoV S protein-based vaccines and drugs will be useful as a model for the development of prophylactic strategies and therapies against other viruses with class I fusion proteins that can cause emerging infectious diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Exp Mol Med
                Journal ID (iso-abbrev): Exp. Mol. Med
                Title: Experimental & Molecular Medicine
                Publisher: Nature Publishing Group
                ISSN (Print): 1226-3613
                ISSN (Electronic): 2092-6413
                Publication date (Print): August 2015
                Publication date (Electronic): 28 August 2015
                Publication date PMC-release: 1 August 2015
                Volume: 47
                Issue: 8
                Page: e181
                Affiliations
                [1 ]Department of Molecular Science and Technology, Ajou University , Suwon, Korea
                Author notes
                [* ]Department of Molecular Science and Technology, Ajou University , Suwon 443-749, Korea. E-mail: sangdunchoi@ 123456ajou.ac.kr
                Article
                Publisher Item ID: emm201576
                DOI: 10.1038/emm.2015.76
                PMC ID: 4558490
                PubMed ID: 26315600
                SO-VID: c0ef93ec-bf91-4326-bae3-697811a34a95
                Copyright © Copyright © 2015 KSBMB.
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 12 July 2015
                Date accepted : 05 August 2015
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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