Viral RNA polymerase complex promotes optimal growth of 1918 virus in the lower respiratory tract of ferrets
Identifieur interne : 004775 ( Main/Merge ); précédent : 004774; suivant : 004776Viral RNA polymerase complex promotes optimal growth of 1918 virus in the lower respiratory tract of ferrets
Auteurs : Tokiko Watanabe [États-Unis] ; Shinji Watanabe [États-Unis] ; Kyoko Shinya [Japon] ; Jin Hyun Kim [États-Unis] ; Masato Hatta [États-Unis] ; Yoshihiro Kawaoka [États-Unis, Japon]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Appareil respiratoire (virologie), Flambées de maladies, Furets, Protéines virales, RNA replicase (physiologie), Réplication virale, Sous-type H1N1 du virus de la grippe A (enzymologie), Sous-type H1N1 du virus de la grippe A (pathogénicité), Sous-type H1N1 du virus de la grippe A (physiologie), Virulence (génétique), Virus de la grippe A (enzymologie), Virus de la grippe A (pathogénicité), Virus de la grippe A (physiologie).
- MESH :
- enzymologie : Sous-type H1N1 du virus de la grippe A, Virus de la grippe A.
- génétique : Virulence.
- pathogénicité : Sous-type H1N1 du virus de la grippe A, Virus de la grippe A.
- physiologie : RNA replicase, Sous-type H1N1 du virus de la grippe A, Virus de la grippe A.
- virologie : Appareil respiratoire.
- Animaux, Flambées de maladies, Furets, Protéines virales, Réplication virale.
English descriptors
- KwdEn :
- Animals, Disease Outbreaks, Ferrets, Influenza A Virus, H1N1 Subtype (enzymology), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza A Virus, H1N1 Subtype (physiology), Influenza A virus (enzymology), Influenza A virus (pathogenicity), Influenza A virus (physiology), RNA Replicase (physiology), Respiratory System (virology), Viral Proteins, Virulence (genetics), Virus Replication.
- MESH :
- chemical , physiology : RNA Replicase.
- enzymology : Influenza A Virus, H1N1 Subtype, Influenza A virus.
- genetics : Virulence.
- pathogenicity : Influenza A Virus, H1N1 Subtype, Influenza A virus.
- physiology : Influenza A Virus, H1N1 Subtype, Influenza A virus.
- virology : Respiratory System.
- Animals, Disease Outbreaks, Ferrets, Viral Proteins, Virus Replication.
Abstract
The 1918 influenza pandemic was the most devastating outbreak of infectious disease in human history, accounting for about 50 million deaths worldwide. In addition to a significant number of cases of secondary bacterial pneumonia, this highly pathogenic strain of influenza A virus caused fatal primary viral pneumonia. To identify the viral gene(s) chiefly responsible for the high virulence of the 1918 virus, we generated a series of reassortants between the 1918 virus and a contemporary human H1N1 virus (A/Kawasaki/173/2001; K173) using reverse genetics. We then assessed their virulence properties in ferrets, a model closely resembling humans in terms of sensitivity to influenza virus infection and pattern of spread after intranasal inoculation. Substitution of single genes from the 1918 virus in the genetic background of K173 virus did not markedly alter the pattern of infection. That is, the reassortants grew well in nasal turbinates, but only sporadically (if at all) in the trachea and lungs. One exception was the 1918PB1/K173 reassortant, which replicated efficiently in lung tissues as well as the upper respiratory tract. A reassortant virus expressing the 1918 viral RNA polymerase complex (PA, PB1, and PB2) and nucleoprotein showed virulence properties in the upper and lower respiratory tracts of ferrets that closely resembled those of wild-type 1918 virus. Our findings strongly implicate the viral RNA polymerase complex as a major determinant of the pathogenicity of the 1918 pandemic virus. This new insight may aid in identifying virulence factors in future pandemic viruses that could be targeted with antiviral compounds.
Url:
DOI: 10.1073/pnas.0806959106
PubMed: 19114663
PubMed Central: 2626747
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id="aff1">Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Wisconsin</region></placeName><wicri:cityArea>Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison</wicri:cityArea></affiliation></author><author><name sortKey="Watanabe, Shinji" sort="Watanabe, Shinji" uniqKey="Watanabe S" first="Shinji" last="Watanabe">Shinji Watanabe</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Wisconsin</region></placeName><wicri:cityArea>Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison</wicri:cityArea></affiliation></author><author><name sortKey="Shinya, Kyoko" sort="Shinya, Kyoko" uniqKey="Shinya K" first="Kyoko" last="Shinya">Kyoko Shinya</name><affiliation wicri:level="1"><nlm:aff wicri:cut="; and" id="aff2">Division of Zoonosis, Department of Microbiology and Infectious Diseases, Graduate School of Medicine, Kobe University, Kobe 650-0017, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Zoonosis, Department of Microbiology and Infectious Diseases, Graduate School of Medicine, Kobe University, Kobe 650-0017</wicri:regionArea><wicri:noRegion>Kobe 650-0017</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Jin Hyun" sort="Kim, Jin Hyun" uniqKey="Kim J" first="Jin Hyun" last="Kim">Jin Hyun Kim</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Wisconsin</region></placeName><wicri:cityArea>Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison</wicri:cityArea></affiliation></author><author><name sortKey="Hatta, Masato" sort="Hatta, Masato" uniqKey="Hatta M" first="Masato" last="Hatta">Masato Hatta</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Wisconsin</region></placeName><wicri:cityArea>Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison</wicri:cityArea></affiliation></author><author><name sortKey="Kawaoka, Yoshihiro" sort="Kawaoka, Yoshihiro" uniqKey="Kawaoka Y" first="Yoshihiro" last="Kawaoka">Yoshihiro Kawaoka</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Wisconsin</region></placeName><wicri:cityArea>Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison</wicri:cityArea><placeName><settlement type="city">Madison (Wisconsin)</settlement><region type="state">Wisconsin</region></placeName><orgName type="university" n="3">Université du Wisconsin à Madison</orgName></affiliation><affiliation wicri:level="1"><nlm:aff wicri:cut="; and" id="aff2">Division of Zoonosis, Department of Microbiology and Infectious Diseases, Graduate School of Medicine, Kobe University, Kobe 650-0017, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Zoonosis, Department of Microbiology and Infectious Diseases, Graduate School of Medicine, Kobe University, Kobe 650-0017</wicri:regionArea><wicri:noRegion>Kobe 650-0017</wicri:noRegion></affiliation><affiliation><nlm:aff wicri:cut=", and" id="aff3">Division of Virology, Department of Microbiology and Immunology</nlm:aff><wicri:noCountry code="subfield">Department of Microbiology and Immunology</wicri:noCountry><country>États-Unis</country><placeName><settlement type="city">Madison (Wisconsin)</settlement><region type="state">Wisconsin</region></placeName><orgName type="university" n="3">Université du Wisconsin à Madison</orgName></affiliation><affiliation wicri:level="4"><nlm:aff id="aff4">International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Tokyo 108-8639</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName><orgName type="university">Université de Tokyo</orgName><placeName><settlement type="city">Tokyo</settlement><region type="province">Région de Kantō</region></placeName><placeName><settlement type="city">Madison (Wisconsin)</settlement><region type="state">Wisconsin</region></placeName><orgName type="university" n="3">Université du Wisconsin à Madison</orgName></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Outbreaks</term><term>Ferrets</term><term>Influenza A Virus, H1N1 Subtype (enzymology)</term><term>Influenza A Virus, H1N1 Subtype (pathogenicity)</term><term>Influenza A Virus, H1N1 Subtype (physiology)</term><term>Influenza A virus (enzymology)</term><term>Influenza A virus (pathogenicity)</term><term>Influenza A virus (physiology)</term><term>RNA Replicase (physiology)</term><term>Respiratory System (virology)</term><term>Viral Proteins</term><term>Virulence (genetics)</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Appareil respiratoire (virologie)</term><term>Flambées de maladies</term><term>Furets</term><term>Protéines virales</term><term>RNA replicase (physiologie)</term><term>Réplication virale</term><term>Sous-type H1N1 du virus de la grippe A (enzymologie)</term><term>Sous-type H1N1 du virus de la grippe A (pathogénicité)</term><term>Sous-type H1N1 du virus de la grippe A (physiologie)</term><term>Virulence (génétique)</term><term>Virus de la grippe A (enzymologie)</term><term>Virus de la grippe A (pathogénicité)</term><term>Virus de la grippe A (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>RNA Replicase</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Virulence</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virulence</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>RNA replicase</term><term>Sous-type H1N1 du virus de la grippe A</term><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Appareil respiratoire</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Respiratory System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Outbreaks</term><term>Ferrets</term><term>Viral Proteins</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Flambées de maladies</term><term>Furets</term><term>Protéines virales</term><term>Réplication virale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The 1918 influenza pandemic was the most devastating outbreak of infectious disease in human history, accounting for about 50 million deaths worldwide. In addition to a significant number of cases of secondary bacterial pneumonia, this highly pathogenic strain of influenza A virus caused fatal primary viral pneumonia. To identify the viral gene(s) chiefly responsible for the high virulence of the 1918 virus, we generated a series of reassortants between the 1918 virus and a contemporary human H1N1 virus (A/Kawasaki/173/2001; K173) using reverse genetics. We then assessed their virulence properties in ferrets, a model closely resembling humans in terms of sensitivity to influenza virus infection and pattern of spread after intranasal inoculation. Substitution of single genes from the 1918 virus in the genetic background of K173 virus did not markedly alter the pattern of infection. That is, the reassortants grew well in nasal turbinates, but only sporadically (if at all) in the trachea and lungs. One exception was the 1918PB1/K173 reassortant, which replicated efficiently in lung tissues as well as the upper respiratory tract. A reassortant virus expressing the 1918 viral RNA polymerase complex (PA, PB1, and PB2) and nucleoprotein showed virulence properties in the upper and lower respiratory tracts of ferrets that closely resembled those of wild-type 1918 virus. Our findings strongly implicate the viral RNA polymerase complex as a major determinant of the pathogenicity of the 1918 pandemic virus. This new insight may aid in identifying virulence factors in future pandemic viruses that could be targeted with antiviral compounds.</p></div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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