Molecular evolution and antigenic variation of European brown hare syndrome virus (EBHSV).
Identifieur interne : 003301 ( PubMed/Corpus ); précédent : 003300; suivant : 003302Molecular evolution and antigenic variation of European brown hare syndrome virus (EBHSV).
Auteurs : Ana M. Lopes ; Lorenzo Capucci ; Dolores Gavier-Widén ; Ghislaine Le Gall-Reculé ; Emiliana Brocchi ; Ilaria Barbieri ; Agnès Quéméner ; Jacques Le Pendu ; Jemma L. Geoghegan ; Edward C. Holmes ; Pedro J. Esteves ; Joana AbrantesSource :
- Virology [ 1096-0341 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Antibodies, Monoclonal, Antibodies, Viral, Antigens, Viral (genetics), Antigens, Viral (metabolism), Bunyaviridae Infections (epidemiology), Bunyaviridae Infections (veterinary), Bunyaviridae Infections (virology), Epitopes (genetics), Evolution, Molecular, Gene Expression Regulation, Viral (physiology), Genetic Variation, Hares (virology), Lagovirus (genetics), Liver (virology), Models, Molecular, Phylogeny, Protein Conformation, Sweden (epidemiology), Time Factors.
- MESH :
- chemical , genetics : Antigens, Viral, Epitopes.
- chemical , metabolism : Antigens, Viral.
- chemical : Antibodies, Monoclonal, Antibodies, Viral.
- geographic , epidemiology : Sweden.
- epidemiology : Bunyaviridae Infections.
- genetics : Lagovirus.
- physiology : Gene Expression Regulation, Viral.
- veterinary : Bunyaviridae Infections.
- virology : Bunyaviridae Infections, Hares, Liver.
- Animals, Evolution, Molecular, Genetic Variation, Models, Molecular, Phylogeny, Protein Conformation, Time Factors.
Abstract
European brown hare syndrome virus (EBHSV) is the aetiological agent of European brown hare syndrome (EBHS), a disease affecting Lepus europaeus and Lepus timidus first diagnosed in Sweden in 1980. To characterize EBHSV evolution we studied hare samples collected in Sweden between 1982 and 2008. Our molecular clock dating is compatible with EBHSV emergence in the 1970s. Phylogenetic analysis revealed two lineages: Group A persisted until 1989 when it apparently suffered extinction; Group B emerged in the mid-1980s and contains the most recent strains. Antigenic differences exist between groups, with loss of reactivity of some MAbs over time, which are associated with amino acid substitutions in recognized epitopes. A role for immune selection is also supported by the presence of positively selected codons in exposed regions of the capsid. Hence, EBHSV evolution is characterized by replacement of Group A by Group B viruses, suggesting that the latter possess a selective advantage.
DOI: 10.1016/j.virol.2014.08.002
PubMed: 25155199
Links to Exploration step
pubmed:25155199Le document en format XML
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<front><div type="abstract" xml:lang="en">European brown hare syndrome virus (EBHSV) is the aetiological agent of European brown hare syndrome (EBHS), a disease affecting Lepus europaeus and Lepus timidus first diagnosed in Sweden in 1980. To characterize EBHSV evolution we studied hare samples collected in Sweden between 1982 and 2008. Our molecular clock dating is compatible with EBHSV emergence in the 1970s. Phylogenetic analysis revealed two lineages: Group A persisted until 1989 when it apparently suffered extinction; Group B emerged in the mid-1980s and contains the most recent strains. Antigenic differences exist between groups, with loss of reactivity of some MAbs over time, which are associated with amino acid substitutions in recognized epitopes. A role for immune selection is also supported by the presence of positively selected codons in exposed regions of the capsid. Hence, EBHSV evolution is characterized by replacement of Group A by Group B viruses, suggesting that the latter possess a selective advantage.</div>
</front>
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<Abstract><AbstractText>European brown hare syndrome virus (EBHSV) is the aetiological agent of European brown hare syndrome (EBHS), a disease affecting Lepus europaeus and Lepus timidus first diagnosed in Sweden in 1980. To characterize EBHSV evolution we studied hare samples collected in Sweden between 1982 and 2008. Our molecular clock dating is compatible with EBHSV emergence in the 1970s. Phylogenetic analysis revealed two lineages: Group A persisted until 1989 when it apparently suffered extinction; Group B emerged in the mid-1980s and contains the most recent strains. Antigenic differences exist between groups, with loss of reactivity of some MAbs over time, which are associated with amino acid substitutions in recognized epitopes. A role for immune selection is also supported by the presence of positively selected codons in exposed regions of the capsid. Hence, EBHSV evolution is characterized by replacement of Group A by Group B viruses, suggesting that the latter possess a selective advantage.</AbstractText>
<CopyrightInformation>Copyright © 2014 Elsevier Inc. All rights reserved.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lopes</LastName>
<ForeName>Ana M</ForeName>
<Initials>AM</Initials>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000911" MajorTopicYN="N">Antibodies, Monoclonal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000914" MajorTopicYN="N">Antibodies, Viral</DescriptorName>
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<MeshHeading><DescriptorName UI="D000956" MajorTopicYN="N">Antigens, Viral</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002044" MajorTopicYN="N">Bunyaviridae Infections</DescriptorName>
<QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName>
<QualifierName UI="Q000662" MajorTopicYN="N">veterinary</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D019143" MajorTopicYN="Y">Evolution, Molecular</DescriptorName>
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<MeshHeading><DescriptorName UI="D034621" MajorTopicYN="N">Hares</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<MeshHeading><DescriptorName UI="D029321" MajorTopicYN="N">Lagovirus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008958" MajorTopicYN="N">Models, Molecular</DescriptorName>
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<MeshHeading><DescriptorName UI="D010802" MajorTopicYN="N">Phylogeny</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011487" MajorTopicYN="N">Protein Conformation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013548" MajorTopicYN="N" Type="Geographic">Sweden</DescriptorName>
<QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName>
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<MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Antigenic variation</Keyword>
<Keyword MajorTopicYN="N">European brown hare syndrome virus (EBHSV)</Keyword>
<Keyword MajorTopicYN="N">Evolution</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year>
<Month>06</Month>
<Day>17</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2014</Year>
<Month>07</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2014</Year>
<Month>08</Month>
<Day>01</Day>
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<PubMedPubDate PubStatus="entrez"><Year>2014</Year>
<Month>8</Month>
<Day>27</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="pubmed"><Year>2014</Year>
<Month>8</Month>
<Day>27</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="medline"><Year>2015</Year>
<Month>2</Month>
<Day>18</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">25155199</ArticleId>
<ArticleId IdType="pii">S0042-6822(14)00373-0</ArticleId>
<ArticleId IdType="doi">10.1016/j.virol.2014.08.002</ArticleId>
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