The genes associated with trans-dominance of the influenza A cold-adapted live virus vaccine.
Identifieur interne : 000447 ( PubMed/Corpus ); précédent : 000446; suivant : 000448The genes associated with trans-dominance of the influenza A cold-adapted live virus vaccine.
Auteurs : P. Whitaker-Dowling ; R. Zvolenski ; J S YoungnerSource :
- Virology [ 0042-6822 ] ; 1991.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Viral Proteins.
- chemical : Vaccines, Attenuated, Viral Vaccines.
- genetics : Influenza A virus, Virus Replication.
- growth & development : Influenza A virus.
- Animals, Cells, Cultured, Chick Embryo, Genes, Viral, Phenotype, Serial Passage, Temperature, Viral Interference.
Abstract
Segment 7 (M) of the cold-adapted live influenza A virus vaccine plays a primary role in the ability of this virus to interfere with the replication of wild-type influenza A viruses. This conclusion is based on several lines of evidence. Single gene reassortant viruses derived by crossing influenza A/Ann Arbor/6/60 (H2N2) cold-adapted donor virus with an epidemic wild-type strain, A/Korea/1/82 (H3N2), were tested for their ability to interfere with wild-type parental virus in the Madin-Darby line of canine kidney cells and embryonated eggs. It was apparent in both hosts that the single gene reassortant carrying segment 7 (M) derived from the cold-adapted virus was dominant over wild-type virus. Additional confirmation of the role of segment 7 (M) in trans-dominance of the cold-adapted vaccine virus was derived from the analysis of reassortants produced by mixed infection by a wild-type virus and its cold-adapted reassortant vaccine strain. After three serial passages, the virus yield contained a high proportion of reassortants carrying segment 7 (M) of the cold-adapted parental strain. When used in mixed infections, these reassortants were dominant over the replication of the parental wild-type virus.
DOI: 10.1016/0042-6822(91)90011-y
PubMed: 1984670
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pubmed:1984670Le document en format XML
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Zvolenski</name></author><author><name sortKey="Youngner, J S" sort="Youngner, J S" uniqKey="Youngner J" first="J S" last="Youngner">J S Youngner</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1991">1991</date><idno type="RBID">pubmed:1984670</idno><idno type="pmid">1984670</idno><idno type="doi">10.1016/0042-6822(91)90011-y</idno><idno type="wicri:Area/PubMed/Corpus">000447</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000447</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The genes associated with trans-dominance of the influenza A cold-adapted live virus vaccine.</title><author><name sortKey="Whitaker Dowling, P" sort="Whitaker Dowling, P" uniqKey="Whitaker Dowling P" first="P" last="Whitaker-Dowling">P. Whitaker-Dowling</name><affiliation><nlm:affiliation>Department of Molecular Genetics and Biochemistry, School of Medicine, University of Pittsburgh, PA 15261.</nlm:affiliation></affiliation></author><author><name sortKey="Zvolenski, R" sort="Zvolenski, R" uniqKey="Zvolenski R" first="R" last="Zvolenski">R. Zvolenski</name></author><author><name sortKey="Youngner, J S" sort="Youngner, J S" uniqKey="Youngner J" first="J S" last="Youngner">J S Youngner</name></author></analytic><series><title level="j">Virology</title><idno type="ISSN">0042-6822</idno><imprint><date when="1991" type="published">1991</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Chick Embryo</term><term>Genes, Viral</term><term>Influenza A virus (genetics)</term><term>Influenza A virus (growth & development)</term><term>Phenotype</term><term>Serial Passage</term><term>Temperature</term><term>Vaccines, Attenuated</term><term>Viral Interference</term><term>Viral Proteins (genetics)</term><term>Viral Vaccines</term><term>Virus Replication (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Vaccines, Attenuated</term><term>Viral Vaccines</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A virus</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Chick Embryo</term><term>Genes, Viral</term><term>Phenotype</term><term>Serial Passage</term><term>Temperature</term><term>Viral Interference</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Segment 7 (M) of the cold-adapted live influenza A virus vaccine plays a primary role in the ability of this virus to interfere with the replication of wild-type influenza A viruses. This conclusion is based on several lines of evidence. Single gene reassortant viruses derived by crossing influenza A/Ann Arbor/6/60 (H2N2) cold-adapted donor virus with an epidemic wild-type strain, A/Korea/1/82 (H3N2), were tested for their ability to interfere with wild-type parental virus in the Madin-Darby line of canine kidney cells and embryonated eggs. It was apparent in both hosts that the single gene reassortant carrying segment 7 (M) derived from the cold-adapted virus was dominant over wild-type virus. Additional confirmation of the role of segment 7 (M) in trans-dominance of the cold-adapted vaccine virus was derived from the analysis of reassortants produced by mixed infection by a wild-type virus and its cold-adapted reassortant vaccine strain. After three serial passages, the virus yield contained a high proportion of reassortants carrying segment 7 (M) of the cold-adapted parental strain. When used in mixed infections, these reassortants were dominant over the replication of the parental wild-type virus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1984670</PMID><DateCompleted><Year>1991</Year><Month>01</Month><Day>29</Day></DateCompleted><DateRevised><Year>2019</Year><Month>07</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0042-6822</ISSN><JournalIssue CitedMedium="Print"><Volume>180</Volume><Issue>1</Issue><PubDate><Year>1991</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Virology</Title><ISOAbbreviation>Virology</ISOAbbreviation></Journal><ArticleTitle>The genes associated with trans-dominance of the influenza A cold-adapted live virus vaccine.</ArticleTitle><Pagination><MedlinePgn>81-7</MedlinePgn></Pagination><Abstract><AbstractText>Segment 7 (M) of the cold-adapted live influenza A virus vaccine plays a primary role in the ability of this virus to interfere with the replication of wild-type influenza A viruses. This conclusion is based on several lines of evidence. Single gene reassortant viruses derived by crossing influenza A/Ann Arbor/6/60 (H2N2) cold-adapted donor virus with an epidemic wild-type strain, A/Korea/1/82 (H3N2), were tested for their ability to interfere with wild-type parental virus in the Madin-Darby line of canine kidney cells and embryonated eggs. It was apparent in both hosts that the single gene reassortant carrying segment 7 (M) derived from the cold-adapted virus was dominant over wild-type virus. Additional confirmation of the role of segment 7 (M) in trans-dominance of the cold-adapted vaccine virus was derived from the analysis of reassortants produced by mixed infection by a wild-type virus and its cold-adapted reassortant vaccine strain. After three serial passages, the virus yield contained a high proportion of reassortants carrying segment 7 (M) of the cold-adapted parental strain. 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