Correlation of pathogenicity and gene constellation of influenza A viruses II. Highly neurovirulent recombinants derived from non-neurovirulent or weakly neurovirulent parent virus strains
Identifieur interne : 002919 ( Main/Exploration ); précédent : 002918; suivant : 002920Correlation of pathogenicity and gene constellation of influenza A viruses II. Highly neurovirulent recombinants derived from non-neurovirulent or weakly neurovirulent parent virus strains
Auteurs : C. Scholtissek [Allemagne] ; Angelika Vallbracht [Allemagne] ; B. Flehmig [Allemagne] ; R. Rott [Allemagne]Source :
- Virology [ 0042-6822 ] ; 1979.
English descriptors
- Teeft :
- Academic press, Certain host, Chick embryo cells, Constellation, Crna, Death time, Double infection, Embryo, Flehmig, Fowl, Gene, Gene constellation, Hemagglutinin, Host range, Human strain, Influenza, Influenza virus, Influenza viruses, Inoculation, Kilbourne, Mouse, Mouse kidney cells, Mouse lungs, Neurovirulence, Neurovirulent, Neurovirulent recombinants, Nonneurovirulent, Other genes, Parent strain, Pathogenicity, Plaque, Plaque formation, Pneumovirulence, Ptra, Ptra gene, Recombinant, Recombinant viruses, Recombination, Rott, Scholtissek, Suckling mice, Vaccine, Vallbracht, Viral, Virology, Virus, Virus dilutions, Virus strains, Vrna, Vrna segments.
Abstract
Abstract: Mixed infections with various nonneurovirulent or weakly neurovirulent influenza A strains yielded recombinants that were highly neurovirulent for mice. A correlation was detected between gene constellation and neurovirulence of these recombinants. For the recombination pair FPV/A2-England the Pol 1 and Ptra genes had to be derived from the human strain; while the HA and/or M gene has to be from FPV in order to obtain highly neurovirulent recombinants. For the FPV/PR8 pair only the Pol 1 gene needs to be derived from PR8 while the HA gene had to be from FPV in order to get highly neurovirulent recombinants. The derivation of the other genes does not appear to be important in this respect. Recombinants between FPV and the A2-Singapore influenza strain do not exhibit significant neurovirulence suggesting that at least one parent strain should be adapted to grow in mice in order to obtain neurovirulent recombinants. In addition, there is a correlation between pneumovirulence and growth in mouse kidney cells, but neurovirulence for mice and pathogenicity for chickens was not correlated. The data presented here demonstrate in principle the possiblity of an increase in pathogenicity in recombinants derived from less or nonpathogenic parent viruses.
Url:
DOI: 10.1016/0042-6822(79)90503-8
Affiliations:
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Rott</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institut für Virologie, Justus-Liebig-Universität Giessen, D-6300 Giessen</wicri:regionArea><wicri:noRegion>D-6300 Giessen</wicri:noRegion><wicri:noRegion>D-6300 Giessen</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="ISSN">0042-6822</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1979">1979</date><biblScope unit="volume">95</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="492">492</biblScope><biblScope unit="page" to="500">500</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Academic press</term><term>Certain host</term><term>Chick embryo cells</term><term>Constellation</term><term>Crna</term><term>Death time</term><term>Double infection</term><term>Embryo</term><term>Flehmig</term><term>Fowl</term><term>Gene</term><term>Gene constellation</term><term>Hemagglutinin</term><term>Host range</term><term>Human strain</term><term>Influenza</term><term>Influenza virus</term><term>Influenza viruses</term><term>Inoculation</term><term>Kilbourne</term><term>Mouse</term><term>Mouse kidney cells</term><term>Mouse lungs</term><term>Neurovirulence</term><term>Neurovirulent</term><term>Neurovirulent recombinants</term><term>Nonneurovirulent</term><term>Other genes</term><term>Parent strain</term><term>Pathogenicity</term><term>Plaque</term><term>Plaque formation</term><term>Pneumovirulence</term><term>Ptra</term><term>Ptra gene</term><term>Recombinant</term><term>Recombinant viruses</term><term>Recombination</term><term>Rott</term><term>Scholtissek</term><term>Suckling mice</term><term>Vaccine</term><term>Vallbracht</term><term>Viral</term><term>Virology</term><term>Virus</term><term>Virus dilutions</term><term>Virus strains</term><term>Vrna</term><term>Vrna segments</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Mixed infections with various nonneurovirulent or weakly neurovirulent influenza A strains yielded recombinants that were highly neurovirulent for mice. A correlation was detected between gene constellation and neurovirulence of these recombinants. For the recombination pair FPV/A2-England the Pol 1 and Ptra genes had to be derived from the human strain; while the HA and/or M gene has to be from FPV in order to obtain highly neurovirulent recombinants. For the FPV/PR8 pair only the Pol 1 gene needs to be derived from PR8 while the HA gene had to be from FPV in order to get highly neurovirulent recombinants. The derivation of the other genes does not appear to be important in this respect. Recombinants between FPV and the A2-Singapore influenza strain do not exhibit significant neurovirulence suggesting that at least one parent strain should be adapted to grow in mice in order to obtain neurovirulent recombinants. In addition, there is a correlation between pneumovirulence and growth in mouse kidney cells, but neurovirulence for mice and pathogenicity for chickens was not correlated. The data presented here demonstrate in principle the possiblity of an increase in pathogenicity in recombinants derived from less or nonpathogenic parent viruses.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Bade-Wurtemberg</li><li>District de Tübingen</li></region><settlement><li>Tübingen</li></settlement></list><tree><country name="Allemagne"><noRegion><name sortKey="Scholtissek, C" sort="Scholtissek, C" uniqKey="Scholtissek C" first="C." last="Scholtissek">C. Scholtissek</name></noRegion><name sortKey="Flehmig, B" sort="Flehmig, B" uniqKey="Flehmig B" first="B." last="Flehmig">B. Flehmig</name><name sortKey="Rott, R" sort="Rott, R" uniqKey="Rott R" first="R." last="Rott">R. Rott</name><name sortKey="Vallbracht, Angelika" sort="Vallbracht, Angelika" uniqKey="Vallbracht A" first="Angelika" last="Vallbracht">Angelika Vallbracht</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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