H2N2V1, PubMed, Curation, bibRecord, 000084

The avian-origin PB1 gene segment facilitated replication and transmissibility of the H3N2/1968 pandemic influenza virus.

Identifieur interne : 000084 ( PubMed/Curation ); précédent : 000083; suivant : 000085

The avian-origin PB1 gene segment facilitated replication and transmissibility of the H3N2/1968 pandemic influenza virus.

Auteurs : Isabel Wendel [Allemagne] ; Dennis Rubbenstroth [Allemagne] ; Jennifer Doedt [Allemagne] ; Georg Kochs [Allemagne] ; Jochen Wilhelm [Allemagne] ; Peter Staeheli [Allemagne] ; Hans-Dieter Klenk [Allemagne] ; Mikhail Matrosovich [Allemagne]

Source :

Journal of virology [ 1098-5514 ] ; 2015.

RBID : pubmed:25631088

Descripteurs français

KwdFr :
- Analyse de séquence d'ADN, Animaux, Cellules HEK293, Cellules rénales canines Madin-Darby, Chiens, Cochons d'Inde, Données de séquences moléculaires, Flambées de maladies (histoire), Grippe chez les oiseaux (transmission), Grippe chez les oiseaux (virologie), Grippe chez les oiseaux (épidémiologie), Grippe humaine (virologie), Grippe humaine (épidémiologie), Génétique inverse, Histoire du 20ème siècle, Humains, Modèles génétiques, Oiseaux, Phylogénie, Protéines virales (génétique), Protéines virales (physiologie), RT-PCR, Sous-type H3N2 du virus de la grippe A, Séquence nucléotidique, Zoonoses (transmission), Zoonoses (virologie), Zoonoses (épidémiologie).
MESH :
- génétique : Protéines virales.
- histoire : Flambées de maladies.
- physiologie : Protéines virales.
- virologie : Grippe chez les oiseaux, Grippe humaine, Zoonoses.
- épidémiologie : Grippe chez les oiseaux, Grippe humaine, Zoonoses.
- Analyse de séquence d'ADN, Animaux, Cellules HEK293, Cellules rénales canines Madin-Darby, Chiens, Cochons d'Inde, Données de séquences moléculaires, Génétique inverse, Histoire du 20ème siècle, Humains, Modèles génétiques, Oiseaux, Phylogénie, RT-PCR, Sous-type H3N2 du virus de la grippe A, Séquence nucléotidique.

English descriptors

KwdEn :
- Animals, Base Sequence, Birds, Disease Outbreaks (history), Dogs, Guinea Pigs, HEK293 Cells, History, 20th Century, Humans, Influenza A Virus, H3N2 Subtype, Influenza in Birds (epidemiology), Influenza in Birds (transmission), Influenza in Birds (virology), Influenza, Human (epidemiology), Influenza, Human (virology), Madin Darby Canine Kidney Cells, Models, Genetic, Molecular Sequence Data, Phylogeny, Reverse Genetics, Reverse Transcriptase Polymerase Chain Reaction, Sequence Analysis, DNA, Viral Proteins (genetics), Viral Proteins (physiology), Zoonoses (epidemiology), Zoonoses (transmission), Zoonoses (virology).
MESH :
- chemical , genetics : Viral Proteins.
- epidemiology : Influenza in Birds, Influenza, Human, Zoonoses.
- history : Disease Outbreaks.
- chemical , physiology : Viral Proteins.
- transmission : Influenza in Birds, Zoonoses.
- virology : Influenza in Birds, Influenza, Human, Zoonoses.
- Animals, Base Sequence, Birds, Dogs, Guinea Pigs, HEK293 Cells, History, 20th Century, Humans, Influenza A Virus, H3N2 Subtype, Madin Darby Canine Kidney Cells, Models, Genetic, Molecular Sequence Data, Phylogeny, Reverse Genetics, Reverse Transcriptase Polymerase Chain Reaction, Sequence Analysis, DNA.

Abstract

The H2N2/1957 and H3N2/1968 pandemic influenza viruses emerged via the exchange of genomic RNA segments between human and avian viruses. The avian hemagglutinin (HA) allowed the hybrid viruses to escape preexisting immunity in the human population. Both pandemic viruses further received the PB1 gene segment from the avian parent (Y. Kawaoka, S. Krauss, and R. G. Webster, J Virol 63:4603-4608, 1989), but the biological significance of this observation was not understood. To assess whether the avian-origin PB1 segment provided pandemic viruses with some selective advantage, either on its own or via cooperation with the homologous HA segment, we modeled by reverse genetics the reassortment event that led to the emergence of the H3N2/1968 pandemic virus. Using seasonal H2N2 virus A/California/1/66 (Cal) as a surrogate precursor human virus and pandemic virus A/Hong Kong/1/68 (H3N2) (HK) as a source of avian-derived PB1 and HA gene segments, we generated four reassortant recombinant viruses and compared pairs of viruses which differed solely by the origin of PB1. Replacement of the PB1 segment of Cal by PB1 of HK facilitated viral polymerase activity, replication efficiency in human cells, and contact transmission in guinea pigs. A combination of PB1 and HA segments of HK did not enhance replicative fitness of the reassortant virus compared with the single-gene PB1 reassortant. Our data suggest that the avian PB1 segment of the 1968 pandemic virus served to enhance viral growth and transmissibility, likely by enhancing activity of the viral polymerase complex.

DOI: 10.1128/JVI.03194-14
PubMed: 25631088

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<front><div type="abstract" xml:lang="en">The H2N2/1957 and H3N2/1968 pandemic influenza viruses emerged via the exchange of genomic RNA segments between human and avian viruses. The avian hemagglutinin (HA) allowed the hybrid viruses to escape preexisting immunity in the human population. Both pandemic viruses further received the PB1 gene segment from the avian parent (Y. Kawaoka, S. Krauss, and R. G. Webster, J Virol 63:4603-4608, 1989), but the biological significance of this observation was not understood. To assess whether the avian-origin PB1 segment provided pandemic viruses with some selective advantage, either on its own or via cooperation with the homologous HA segment, we modeled by reverse genetics the reassortment event that led to the emergence of the H3N2/1968 pandemic virus. Using seasonal H2N2 virus A/California/1/66 (Cal) as a surrogate precursor human virus and pandemic virus A/Hong Kong/1/68 (H3N2) (HK) as a source of avian-derived PB1 and HA gene segments, we generated four reassortant recombinant viruses and compared pairs of viruses which differed solely by the origin of PB1. Replacement of the PB1 segment of Cal by PB1 of HK facilitated viral polymerase activity, replication efficiency in human cells, and contact transmission in guinea pigs. A combination of PB1 and HA segments of HK did not enhance replicative fitness of the reassortant virus compared with the single-gene PB1 reassortant. Our data suggest that the avian PB1 segment of the 1968 pandemic virus served to enhance viral growth and transmissibility, likely by enhancing activity of the viral polymerase complex.</div>
</front>
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<DateCompleted><Year>2015</Year>
<Month>05</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>89</Volume>
<Issue>8</Issue>
<PubDate><Year>2015</Year>
<Month>Apr</Month>
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<Title>Journal of virology</Title>
<ISOAbbreviation>J. Virol.</ISOAbbreviation>
</Journal>
<ArticleTitle>The avian-origin PB1 gene segment facilitated replication and transmissibility of the H3N2/1968 pandemic influenza virus.</ArticleTitle>
<Pagination><MedlinePgn>4170-9</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.03194-14</ELocationID>
<Abstract><AbstractText Label="UNLABELLED">The H2N2/1957 and H3N2/1968 pandemic influenza viruses emerged via the exchange of genomic RNA segments between human and avian viruses. The avian hemagglutinin (HA) allowed the hybrid viruses to escape preexisting immunity in the human population. Both pandemic viruses further received the PB1 gene segment from the avian parent (Y. Kawaoka, S. Krauss, and R. G. Webster, J Virol 63:4603-4608, 1989), but the biological significance of this observation was not understood. To assess whether the avian-origin PB1 segment provided pandemic viruses with some selective advantage, either on its own or via cooperation with the homologous HA segment, we modeled by reverse genetics the reassortment event that led to the emergence of the H3N2/1968 pandemic virus. Using seasonal H2N2 virus A/California/1/66 (Cal) as a surrogate precursor human virus and pandemic virus A/Hong Kong/1/68 (H3N2) (HK) as a source of avian-derived PB1 and HA gene segments, we generated four reassortant recombinant viruses and compared pairs of viruses which differed solely by the origin of PB1. Replacement of the PB1 segment of Cal by PB1 of HK facilitated viral polymerase activity, replication efficiency in human cells, and contact transmission in guinea pigs. A combination of PB1 and HA segments of HK did not enhance replicative fitness of the reassortant virus compared with the single-gene PB1 reassortant. Our data suggest that the avian PB1 segment of the 1968 pandemic virus served to enhance viral growth and transmissibility, likely by enhancing activity of the viral polymerase complex.</AbstractText>
<AbstractText Label="IMPORTANCE" NlmCategory="OBJECTIVE">Despite the high impact of influenza pandemics on human health, some mechanisms underlying the emergence of pandemic influenza viruses still are poorly understood. Thus, it was unclear why both H2N2/1957 and H3N2/1968 reassortant pandemic viruses contained, in addition to the avian HA, the PB1 gene segment of the avian parent. Here, we addressed this long-standing question by modeling the emergence of the H3N2/1968 virus from its putative human and avian precursors. We show that the avian PB1 segment increased activity of the viral polymerase and facilitated viral replication. Our results suggest that in addition to the acquisition of antigenically novel HA (i.e., antigenic shift), enhanced viral polymerase activity is required for the emergence of pandemic influenza viruses from their seasonal human precursors.</AbstractText>
<CopyrightInformation>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wendel</LastName>
<ForeName>Isabel</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Institute of Virology, Philipps University, Marburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rubbenstroth</LastName>
<ForeName>Dennis</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Institute of Virology, University Medical Center Freiburg, Freiburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Doedt</LastName>
<ForeName>Jennifer</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Institute of Virology, Philipps University, Marburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kochs</LastName>
<ForeName>Georg</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Institute of Virology, University Medical Center Freiburg, Freiburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wilhelm</LastName>
<ForeName>Jochen</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>German Lung Research Center, Justus Liebig University, Giessen, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Staeheli</LastName>
<ForeName>Peter</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Institute of Virology, University Medical Center Freiburg, Freiburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Klenk</LastName>
<ForeName>Hans-Dieter</ForeName>
<Initials>HD</Initials>
<AffiliationInfo><Affiliation>Institute of Virology, Philipps University, Marburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Matrosovich</LastName>
<ForeName>Mikhail</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Institute of Virology, Philipps University, Marburg, Germany matrosov@staff.uni-marburg.de.</Affiliation>
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The avian-origin PB1 gene segment facilitated replication and transmissibility of the H3N2/1968 pandemic influenza virus.

The avian-origin PB1 gene segment facilitated replication and transmissibility of the H3N2/1968 pandemic influenza virus.

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