The heptad repeat region is a major selection target in MERS-CoV and related coronaviruses.
Identifieur interne : 001459 ( PubMed/Corpus ); précédent : 001458; suivant : 001460The heptad repeat region is a major selection target in MERS-CoV and related coronaviruses.
Auteurs : Diego Forni ; Giulia Filippi ; Rachele Cagliani ; Luca De Gioia ; Uberto Pozzoli ; Nasser Al-Daghri ; Mario Clerici ; Manuela SironiSource :
- Scientific reports [ 2045-2322 ] ; 2015.
English descriptors
- KwdEn :
- Amino Acid Sequence, Animals, Coronavirus (genetics), Evolution, Molecular, Genes, Viral, Genetic Variation, Genotype, Humans, Middle East Respiratory Syndrome Coronavirus (genetics), Molecular Sequence Data, Phylogeny, Recombination, Genetic, Repetitive Sequences, Nucleic Acid, Selection, Genetic, Sequence Alignment.
- MESH :
- genetics : Coronavirus, Middle East Respiratory Syndrome Coronavirus.
- Amino Acid Sequence, Animals, Evolution, Molecular, Genes, Viral, Genetic Variation, Genotype, Humans, Molecular Sequence Data, Phylogeny, Recombination, Genetic, Repetitive Sequences, Nucleic Acid, Selection, Genetic, Sequence Alignment.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) originated in bats and spread to humans via zoonotic transmission from camels. We analyzed the evolution of the spike (S) gene in betacoronaviruses (betaCoVs) isolated from different mammals, in bat coronavirus populations, as well as in MERS-CoV strains from the current outbreak. Results indicated several positively selected sites located in the region comprising the two heptad repeats (HR1 and HR2) and their linker. Two sites (R652 and V1060) were positively selected in the betaCoVs phylogeny and correspond to mutations associated with expanded host range in other coronaviruses. During the most recent evolution of MERS-CoV, adaptive mutations in the HR1 (Q/R/H1020) arose in camels or in a previous host and spread to humans. We determined that different residues at position 1020 establish distinct inter- and intra-helical interactions and affect the stability of the six-helix bundle formed by the HRs. A similar effect on stability was observed for a nearby mutation (T1015N) that increases MERS-CoV infection efficiency in vitro. Data herein indicate that the heptad repeat region was a major target of adaptive evolution in MERS-CoV-related viruses; these results are relevant for the design of fusion inhibitor peptides with antiviral function.
DOI: 10.1038/srep14480
PubMed: 26404138
Links to Exploration step
pubmed:26404138Le document en format XML
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MEDEA, Bioinformatics, 23842 Bosisio Parini, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Filippi, Giulia" sort="Filippi, Giulia" uniqKey="Filippi G" first="Giulia" last="Filippi">Giulia Filippi</name><affiliation><nlm:affiliation>Department of Biotechnology and Biosciences, University of Milan-Bicocca, 20126 Milan, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Cagliani, Rachele" sort="Cagliani, Rachele" uniqKey="Cagliani R" first="Rachele" last="Cagliani">Rachele Cagliani</name><affiliation><nlm:affiliation>Scientific Institute IRCCS E. MEDEA, Bioinformatics, 23842 Bosisio Parini, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="De Gioia, Luca" sort="De Gioia, Luca" uniqKey="De Gioia L" first="Luca" last="De Gioia">Luca De Gioia</name><affiliation><nlm:affiliation>Department of Biotechnology and Biosciences, University of Milan-Bicocca, 20126 Milan, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Pozzoli, Uberto" sort="Pozzoli, Uberto" uniqKey="Pozzoli U" first="Uberto" last="Pozzoli">Uberto Pozzoli</name><affiliation><nlm:affiliation>Scientific Institute IRCCS E. MEDEA, Bioinformatics, 23842 Bosisio Parini, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Al Daghri, Nasser" sort="Al Daghri, Nasser" uniqKey="Al Daghri N" first="Nasser" last="Al-Daghri">Nasser Al-Daghri</name><affiliation><nlm:affiliation>Biomarkers research program, Biochemistry Department, College of Science, King Saud University, Riyadh 11451, Kingdom of Saudi Arabia (KSA).</nlm:affiliation></affiliation></author><author><name sortKey="Clerici, Mario" sort="Clerici, Mario" uniqKey="Clerici M" first="Mario" last="Clerici">Mario Clerici</name><affiliation><nlm:affiliation>Department of Physiopathology and Transplantation, University of Milan, 20090 Milan, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Sironi, Manuela" sort="Sironi, Manuela" uniqKey="Sironi M" first="Manuela" last="Sironi">Manuela Sironi</name><affiliation><nlm:affiliation>Scientific Institute IRCCS E. MEDEA, Bioinformatics, 23842 Bosisio Parini, Italy.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Coronavirus (genetics)</term><term>Evolution, Molecular</term><term>Genes, Viral</term><term>Genetic Variation</term><term>Genotype</term><term>Humans</term><term>Middle East Respiratory Syndrome Coronavirus (genetics)</term><term>Molecular Sequence Data</term><term>Phylogeny</term><term>Recombination, Genetic</term><term>Repetitive Sequences, Nucleic Acid</term><term>Selection, Genetic</term><term>Sequence Alignment</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Coronavirus</term><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Evolution, Molecular</term><term>Genes, Viral</term><term>Genetic Variation</term><term>Genotype</term><term>Humans</term><term>Molecular Sequence Data</term><term>Phylogeny</term><term>Recombination, Genetic</term><term>Repetitive Sequences, Nucleic Acid</term><term>Selection, Genetic</term><term>Sequence Alignment</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Middle East respiratory syndrome coronavirus (MERS-CoV) originated in bats and spread to humans via zoonotic transmission from camels. We analyzed the evolution of the spike (S) gene in betacoronaviruses (betaCoVs) isolated from different mammals, in bat coronavirus populations, as well as in MERS-CoV strains from the current outbreak. Results indicated several positively selected sites located in the region comprising the two heptad repeats (HR1 and HR2) and their linker. Two sites (R652 and V1060) were positively selected in the betaCoVs phylogeny and correspond to mutations associated with expanded host range in other coronaviruses. During the most recent evolution of MERS-CoV, adaptive mutations in the HR1 (Q/R/H1020) arose in camels or in a previous host and spread to humans. We determined that different residues at position 1020 establish distinct inter- and intra-helical interactions and affect the stability of the six-helix bundle formed by the HRs. A similar effect on stability was observed for a nearby mutation (T1015N) that increases MERS-CoV infection efficiency in vitro. Data herein indicate that the heptad repeat region was a major target of adaptive evolution in MERS-CoV-related viruses; these results are relevant for the design of fusion inhibitor peptides with antiviral function.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26404138</PMID><DateCompleted><Year>2016</Year><Month>08</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><PubDate><Year>2015</Year><Month>Sep</Month><Day>25</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>The heptad repeat region is a major selection target in MERS-CoV and related coronaviruses.</ArticleTitle><Pagination><MedlinePgn>14480</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/srep14480</ELocationID><Abstract><AbstractText>Middle East respiratory syndrome coronavirus (MERS-CoV) originated in bats and spread to humans via zoonotic transmission from camels. We analyzed the evolution of the spike (S) gene in betacoronaviruses (betaCoVs) isolated from different mammals, in bat coronavirus populations, as well as in MERS-CoV strains from the current outbreak. Results indicated several positively selected sites located in the region comprising the two heptad repeats (HR1 and HR2) and their linker. Two sites (R652 and V1060) were positively selected in the betaCoVs phylogeny and correspond to mutations associated with expanded host range in other coronaviruses. During the most recent evolution of MERS-CoV, adaptive mutations in the HR1 (Q/R/H1020) arose in camels or in a previous host and spread to humans. We determined that different residues at position 1020 establish distinct inter- and intra-helical interactions and affect the stability of the six-helix bundle formed by the HRs. A similar effect on stability was observed for a nearby mutation (T1015N) that increases MERS-CoV infection efficiency in vitro. Data herein indicate that the heptad repeat region was a major target of adaptive evolution in MERS-CoV-related viruses; these results are relevant for the design of fusion inhibitor peptides with antiviral function.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Forni</LastName><ForeName>Diego</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Scientific Institute IRCCS E. MEDEA, Bioinformatics, 23842 Bosisio Parini, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Filippi</LastName><ForeName>Giulia</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Biotechnology and Biosciences, University of Milan-Bicocca, 20126 Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cagliani</LastName><ForeName>Rachele</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Scientific Institute IRCCS E. MEDEA, Bioinformatics, 23842 Bosisio Parini, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>De Gioia</LastName><ForeName>Luca</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Biotechnology and Biosciences, University of Milan-Bicocca, 20126 Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pozzoli</LastName><ForeName>Uberto</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Scientific Institute IRCCS E. MEDEA, Bioinformatics, 23842 Bosisio Parini, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Daghri</LastName><ForeName>Nasser</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Biomarkers research program, Biochemistry Department, College of Science, King Saud University, Riyadh 11451, Kingdom of Saudi Arabia (KSA).</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Prince Mutaib Chair for Biomarkers of Osteoporosis, Biochemistry Department, College of science, King Saud University, Riyadh, KSA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Clerici</LastName><ForeName>Mario</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Physiopathology and Transplantation, University of Milan, 20090 Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Don C. Gnocchi Foundation ONLUS, IRCCS, 20148 Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sironi</LastName><ForeName>Manuela</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Scientific Institute IRCCS E. 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