Amino acids adjacent to the haemagglutinin cleavage site are relevant for virulence of avian influenza viruses of subtype H5.
Identifieur interne : 000306 ( Main/Exploration ); précédent : 000305; suivant : 000307Amino acids adjacent to the haemagglutinin cleavage site are relevant for virulence of avian influenza viruses of subtype H5.
Auteurs : Sandra Gohrbandt [Allemagne] ; Jutta Veits ; Jana Hundt ; Jessica Bogs ; Angele Breithaupt ; Jens P. Teifke ; Siegfried Weber ; Thomas C. Mettenleiter ; Jürgen StechSource :
- The Journal of general virology [ 1465-2099 ] ; 2011.
Descripteurs français
- KwdFr :
- Allemagne (MeSH), Analyse de survie (MeSH), Animaux (MeSH), Appareil respiratoire (anatomopathologie), Appareil respiratoire (virologie), Grippe chez les oiseaux (anatomopathologie), Grippe chez les oiseaux (mortalité), Grippe chez les oiseaux (virologie), Hémagglutinines virales (génétique), Hémagglutinines virales (métabolisme), Motifs d'acides aminés (génétique), Mutagenèse par insertion (MeSH), Mutation faux-sens (MeSH), Poulets (MeSH), Sous-type H5N1 du virus de la grippe A (génétique), Sous-type H5N1 du virus de la grippe A (pathogénicité), Substitution d'acide aminé (génétique), Virulence (MeSH).
- MESH :
- anatomopathologie : Appareil respiratoire, Grippe chez les oiseaux.
- génétique : Hémagglutinines virales, Motifs d'acides aminés, Sous-type H5N1 du virus de la grippe A, Substitution d'acide aminé.
- mortalité : Grippe chez les oiseaux.
- métabolisme : Hémagglutinines virales.
- pathogénicité : Sous-type H5N1 du virus de la grippe A.
- virologie : Appareil respiratoire, Grippe chez les oiseaux.
- Allemagne, Analyse de survie, Animaux, Mutagenèse par insertion, Mutation faux-sens, Poulets, Virulence.
- Wicri :
- geographic : Allemagne.
English descriptors
- KwdEn :
- Amino Acid Motifs (genetics), Amino Acid Substitution (genetics), Animals (MeSH), Chickens (MeSH), Germany (MeSH), Hemagglutinins, Viral (genetics), Hemagglutinins, Viral (metabolism), Influenza A Virus, H5N1 Subtype (genetics), Influenza A Virus, H5N1 Subtype (pathogenicity), Influenza in Birds (mortality), Influenza in Birds (pathology), Influenza in Birds (virology), Mutagenesis, Insertional (MeSH), Mutation, Missense (MeSH), Respiratory System (pathology), Respiratory System (virology), Survival Analysis (MeSH), Virulence (MeSH).
- MESH :
- chemical , genetics : Hemagglutinins, Viral.
- chemical , metabolism : Hemagglutinins, Viral.
- geographic : Germany.
- genetics : Amino Acid Motifs, Amino Acid Substitution, Influenza A Virus, H5N1 Subtype.
- mortality : Influenza in Birds.
- pathogenicity : Influenza A Virus, H5N1 Subtype.
- pathology : Influenza in Birds, Respiratory System.
- virology : Influenza in Birds, Respiratory System.
- Animals, Chickens, Mutagenesis, Insertional, Mutation, Missense, Survival Analysis, Virulence.
Abstract
The prime virulence determinant of highly pathogenic avian influenza viruses (HPAIVs) is the polybasic haemagglutinin (HA) cleavage site. However, engineering of a polybasic cleavage site into an avian influenza virus of low pathogenicity does not result in transformation into an HPAIV, indicating the importance of other adaptations. Here, the influence of amino acids adjacent to the HA cleavage site on virulence was studied. Most HPAIVs of subtype H5 carry serine or threonine at position 346 (corresponding to position 323 according to H3 numbering), whereas almost all low-pathogenic H5 viruses have valine. Moreover, all H5 low-pathogenic strains carry threonine at position 351 (corresponding to position 328 according to H3 numbering), suggesting that acquisition of a polybasic cleavage site involves several steps. This study generated a virus mutant derived from HPAIV A/Swan/Germany/R65/06 H5N1 (R65) with a monobasic cleavage site, R65(mono)-S-ER, and the following additional mutants: R65(mono)-V-ER with serine changed to valine at position 346, and R65(mono)-S-ETR and R65(mono)-V-ETR with threonine inserted at position 351. Moreover, in the R65 HA, serine was replaced with valine at position 346 (R65-V). Infection of chickens with R65(mono)-S-ETR or R65(mono)-S-ER led to slight transient respiratory symptoms, whereas R65-infected animals died within 2 days. However, chickens infected with R65-V survived longer than R65-infected animals, indicating that serine 346 in R65 HA contributes to virulence. These data suggest that evolution of H5 HPAIVs from low-pathogenic precursors, besides acquisition of a polybasic cleavage site, involves adaptation of neighbouring regions.
DOI: 10.1099/vir.0.023887-0
PubMed: 20881092
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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However, engineering of a polybasic cleavage site into an avian influenza virus of low pathogenicity does not result in transformation into an HPAIV, indicating the importance of other adaptations. Here, the influence of amino acids adjacent to the HA cleavage site on virulence was studied. Most HPAIVs of subtype H5 carry serine or threonine at position 346 (corresponding to position 323 according to H3 numbering), whereas almost all low-pathogenic H5 viruses have valine. Moreover, all H5 low-pathogenic strains carry threonine at position 351 (corresponding to position 328 according to H3 numbering), suggesting that acquisition of a polybasic cleavage site involves several steps. This study generated a virus mutant derived from HPAIV A/Swan/Germany/R65/06 H5N1 (R65) with a monobasic cleavage site, R65(mono)-S-ER, and the following additional mutants: R65(mono)-V-ER with serine changed to valine at position 346, and R65(mono)-S-ETR and R65(mono)-V-ETR with threonine inserted at position 351. Moreover, in the R65 HA, serine was replaced with valine at position 346 (R65-V). Infection of chickens with R65(mono)-S-ETR or R65(mono)-S-ER led to slight transient respiratory symptoms, whereas R65-infected animals died within 2 days. However, chickens infected with R65-V survived longer than R65-infected animals, indicating that serine 346 in R65 HA contributes to virulence. These data suggest that evolution of H5 HPAIVs from low-pathogenic precursors, besides acquisition of a polybasic cleavage site, involves adaptation of neighbouring regions.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20881092</PMID><DateCompleted><Year>2011</Year><Month>01</Month><Day>18</Day></DateCompleted><DateRevised><Year>2010</Year><Month>12</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>92</Volume><Issue>Pt 1</Issue><PubDate><Year>2011</Year><Month>Jan</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J. Gen. Virol.</ISOAbbreviation></Journal><ArticleTitle>Amino acids adjacent to the haemagglutinin cleavage site are relevant for virulence of avian influenza viruses of subtype H5.</ArticleTitle><Pagination><MedlinePgn>51-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/vir.0.023887-0</ELocationID><Abstract><AbstractText>The prime virulence determinant of highly pathogenic avian influenza viruses (HPAIVs) is the polybasic haemagglutinin (HA) cleavage site. However, engineering of a polybasic cleavage site into an avian influenza virus of low pathogenicity does not result in transformation into an HPAIV, indicating the importance of other adaptations. Here, the influence of amino acids adjacent to the HA cleavage site on virulence was studied. Most HPAIVs of subtype H5 carry serine or threonine at position 346 (corresponding to position 323 according to H3 numbering), whereas almost all low-pathogenic H5 viruses have valine. Moreover, all H5 low-pathogenic strains carry threonine at position 351 (corresponding to position 328 according to H3 numbering), suggesting that acquisition of a polybasic cleavage site involves several steps. This study generated a virus mutant derived from HPAIV A/Swan/Germany/R65/06 H5N1 (R65) with a monobasic cleavage site, R65(mono)-S-ER, and the following additional mutants: R65(mono)-V-ER with serine changed to valine at position 346, and R65(mono)-S-ETR and R65(mono)-V-ETR with threonine inserted at position 351. Moreover, in the R65 HA, serine was replaced with valine at position 346 (R65-V). Infection of chickens with R65(mono)-S-ETR or R65(mono)-S-ER led to slight transient respiratory symptoms, whereas R65-infected animals died within 2 days. However, chickens infected with R65-V survived longer than R65-infected animals, indicating that serine 346 in R65 HA contributes to virulence. These data suggest that evolution of H5 HPAIVs from low-pathogenic precursors, besides acquisition of a polybasic cleavage site, involves adaptation of neighbouring regions.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gohrbandt</LastName><ForeName>Sandra</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Friedrich-Loeffler-Institut, Institute of Molecular Biology, Greifswald-Insel Riems, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Veits</LastName><ForeName>Jutta</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Hundt</LastName><ForeName>Jana</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Bogs</LastName><ForeName>Jessica</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Breithaupt</LastName><ForeName>Angele</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Teifke</LastName><ForeName>Jens P</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>Weber</LastName><ForeName>Siegfried</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Mettenleiter</LastName><ForeName>Thomas C</ForeName><Initials>TC</Initials></Author><Author ValidYN="Y"><LastName>Stech</LastName><ForeName>Jürgen</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Gen Virol</MedlineTA><NlmUniqueID>0077340</NlmUniqueID><ISSNLinking>0022-1317</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006389">Hemagglutinins, Viral</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C458881">hemagglutinin fusogenic peptide, influenza virus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D020816" MajorTopicYN="N">Amino Acid Motifs</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019943" MajorTopicYN="N">Amino Acid Substitution</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002645" MajorTopicYN="N">Chickens</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005858" MajorTopicYN="N" Type="Geographic">Germany</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006389" MajorTopicYN="N">Hemagglutinins, Viral</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053124" MajorTopicYN="N">Influenza A Virus, H5N1 Subtype</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005585" MajorTopicYN="N">Influenza in Birds</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016254" MajorTopicYN="N">Mutagenesis, Insertional</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020125" MajorTopicYN="N">Mutation, Missense</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012137" MajorTopicYN="N">Respiratory System</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016019" MajorTopicYN="N">Survival Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>1</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20881092</ArticleId><ArticleId IdType="pii">vir.0.023887-0</ArticleId><ArticleId IdType="doi">10.1099/vir.0.023887-0</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country></list><tree><noCountry><name sortKey="Bogs, Jessica" sort="Bogs, Jessica" uniqKey="Bogs J" first="Jessica" last="Bogs">Jessica Bogs</name><name sortKey="Breithaupt, Angele" sort="Breithaupt, Angele" uniqKey="Breithaupt A" first="Angele" last="Breithaupt">Angele Breithaupt</name><name sortKey="Hundt, Jana" sort="Hundt, Jana" uniqKey="Hundt J" first="Jana" last="Hundt">Jana Hundt</name><name sortKey="Mettenleiter, Thomas C" sort="Mettenleiter, Thomas C" uniqKey="Mettenleiter T" first="Thomas C" last="Mettenleiter">Thomas C. Mettenleiter</name><name sortKey="Stech, Jurgen" sort="Stech, Jurgen" uniqKey="Stech J" first="Jürgen" last="Stech">Jürgen Stech</name><name sortKey="Teifke, Jens P" sort="Teifke, Jens P" uniqKey="Teifke J" first="Jens P" last="Teifke">Jens P. Teifke</name><name sortKey="Veits, Jutta" sort="Veits, Jutta" uniqKey="Veits J" first="Jutta" last="Veits">Jutta Veits</name><name sortKey="Weber, Siegfried" sort="Weber, Siegfried" uniqKey="Weber S" first="Siegfried" last="Weber">Siegfried Weber</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Gohrbandt, Sandra" sort="Gohrbandt, Sandra" uniqKey="Gohrbandt S" first="Sandra" last="Gohrbandt">Sandra Gohrbandt</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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