Coronavirus Spike Protein and Tropism Changes
Identifieur interne : 000C13 ( Pmc/Checkpoint ); précédent : 000C12; suivant : 000C14Coronavirus Spike Protein and Tropism Changes
Auteurs : R. J. G. Hulswit ; C. A. M. De Haan ; B.-J. BoschSource :
- Advances in Virus Research [ 0065-3527 ] ; 2016.
Abstract
Coronaviruses (CoVs) have a remarkable potential to change tropism. This is particularly illustrated over the last 15 years by the emergence of two zoonotic CoVs, the severe acute respiratory syndrome (SARS)- and Middle East respiratory syndrome (MERS)-CoV. Due to their inherent genetic variability, it is inevitable that new cross-species transmission events of these enveloped, positive-stranded RNA viruses will occur. Research into these medical and veterinary important pathogens—sparked by the SARS and MERS outbreaks—revealed important principles of inter- and intraspecies tropism changes. The primary determinant of CoV tropism is the viral spike (S) entry protein. Trimers of the S glycoproteins on the virion surface accommodate binding to a cell surface receptor and fusion of the viral and cellular membrane. Recently, high-resolution structures of two CoV S proteins have been elucidated by single-particle cryo-electron microscopy. Using this new structural insight, we review the changes in the S protein that relate to changes in virus tropism. Different concepts underlie these tropism changes at the cellular, tissue, and host species level, including the promiscuity or adaptability of S proteins to orthologous receptors, alterations in the proteolytic cleavage activation as well as changes in the S protein metastability. A thorough understanding of the key role of the S protein in CoV entry is critical to further our understanding of virus cross-species transmission and pathogenesis and for development of intervention strategies.
Url:
DOI: 10.1016/bs.aivir.2016.08.004
PubMed: 27712627
PubMed Central: 7112277
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Coronaviruses (CoVs) have a remarkable potential to change tropism. This is particularly illustrated over the last 15 years by the emergence of two zoonotic CoVs, the severe acute respiratory syndrome (SARS)- and Middle East respiratory syndrome (MERS)-CoV. Due to their inherent genetic variability, it is inevitable that new cross-species transmission events of these enveloped, positive-stranded RNA viruses will occur. Research into these medical and veterinary important pathogens—sparked by the SARS and MERS outbreaks—revealed important principles of inter- and intraspecies tropism changes. The primary determinant of CoV tropism is the viral spike (S) entry protein. Trimers of the S glycoproteins on the virion surface accommodate binding to a cell surface receptor and fusion of the viral and cellular membrane. Recently, high-resolution structures of two CoV S proteins have been elucidated by single-particle cryo-electron microscopy. Using this new structural insight, we review the changes in the S protein that relate to changes in virus tropism. Different concepts underlie these tropism changes at the cellular, tissue, and host species level, including the promiscuity or adaptability of S proteins to orthologous receptors, alterations in the proteolytic cleavage activation as well as changes in the S protein metastability. A thorough understanding of the key role of the S protein in CoV entry is critical to further our understanding of virus cross-species transmission and pathogenesis and for development of intervention strategies.</p>
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<pmc article-type="other"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Adv Virus Res</journal-id>
<journal-id journal-id-type="iso-abbrev">Adv. Virus Res</journal-id>
<journal-title-group><journal-title>Advances in Virus Research</journal-title>
</journal-title-group>
<issn pub-type="ppub">0065-3527</issn>
<issn pub-type="epub">1557-8399</issn>
<publisher><publisher-name>Elsevier Inc.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">27712627</article-id>
<article-id pub-id-type="pmc">7112277</article-id>
<article-id pub-id-type="publisher-id">S0065-3527(16)30043-4</article-id>
<article-id pub-id-type="doi">10.1016/bs.aivir.2016.08.004</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Coronavirus Spike Protein and Tropism Changes</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" id="au0005"><name><surname>Hulswit</surname>
<given-names>R.J.G.</given-names>
</name>
</contrib>
<contrib contrib-type="author" id="au0010"><name><surname>de Haan</surname>
<given-names>C.A.M.</given-names>
</name>
<email>c.a.m.dehaan@uu.nl</email>
<xref rid="cr0005" ref-type="corresp">1</xref>
</contrib>
<contrib contrib-type="author" id="au0015"><name><surname>Bosch</surname>
<given-names>B.-J.</given-names>
</name>
<email>b.j.bosch@uu.nl</email>
<xref rid="cr0005" ref-type="corresp">1</xref>
</contrib>
</contrib-group>
<aff id="af0005">Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands</aff>
<author-notes><corresp id="cr0005"><label>1</label>
Corresponding authors: <email>c.a.m.dehaan@uu.nl</email>
<email>b.j.bosch@uu.nl</email>
</corresp>
</author-notes>
<pub-date pub-type="pmc-release"><day>13</day>
<month>9</month>
<year>2016</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><year>2016</year>
</pub-date>
<pub-date pub-type="epub"><day>13</day>
<month>9</month>
<year>2016</year>
</pub-date>
<volume>96</volume>
<fpage>29</fpage>
<lpage>57</lpage>
<permissions><copyright-statement>Copyright © 2016 Elsevier Inc. All rights reserved.</copyright-statement>
<copyright-year>2016</copyright-year>
<copyright-holder>Elsevier Inc.</copyright-holder>
<license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p>
</license>
</permissions>
<abstract id="ab0005"><p>Coronaviruses (CoVs) have a remarkable potential to change tropism. This is particularly illustrated over the last 15 years by the emergence of two zoonotic CoVs, the severe acute respiratory syndrome (SARS)- and Middle East respiratory syndrome (MERS)-CoV. Due to their inherent genetic variability, it is inevitable that new cross-species transmission events of these enveloped, positive-stranded RNA viruses will occur. Research into these medical and veterinary important pathogens—sparked by the SARS and MERS outbreaks—revealed important principles of inter- and intraspecies tropism changes. The primary determinant of CoV tropism is the viral spike (S) entry protein. Trimers of the S glycoproteins on the virion surface accommodate binding to a cell surface receptor and fusion of the viral and cellular membrane. Recently, high-resolution structures of two CoV S proteins have been elucidated by single-particle cryo-electron microscopy. Using this new structural insight, we review the changes in the S protein that relate to changes in virus tropism. Different concepts underlie these tropism changes at the cellular, tissue, and host species level, including the promiscuity or adaptability of S proteins to orthologous receptors, alterations in the proteolytic cleavage activation as well as changes in the S protein metastability. A thorough understanding of the key role of the S protein in CoV entry is critical to further our understanding of virus cross-species transmission and pathogenesis and for development of intervention strategies.</p>
</abstract>
<kwd-group id="ks0005"><title>Keywords</title>
<kwd>Coronavirus spike</kwd>
<kwd>Tropism</kwd>
<kwd>Cross-species transmission</kwd>
<kwd>Receptor interaction</kwd>
<kwd>Membrane fusion</kwd>
<kwd>Cryo-EM structure</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Bosch, B J" sort="Bosch, B J" uniqKey="Bosch B" first="B.-J." last="Bosch">B.-J. Bosch</name>
<name sortKey="De Haan, C A M" sort="De Haan, C A M" uniqKey="De Haan C" first="C. A. M." last="De Haan">C. A. M. De Haan</name>
<name sortKey="Hulswit, R J G" sort="Hulswit, R J G" uniqKey="Hulswit R" first="R. J. G." last="Hulswit">R. J. G. Hulswit</name>
</noCountry>
</tree>
</affiliations>
</record>
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