Serveur d'exploration H2N2

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Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia

Identifieur interne : 000067 ( PascalFrancis/Curation ); précédent : 000066; suivant : 000068

Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia

Auteurs : Ashok K. Chockalingam [États-Unis] ; Danielle Hickman [États-Unis] ; Lindomar Pena [États-Unis] ; JIANQIANG YE [États-Unis] ; Andrea Ferrero [États-Unis] ; Jose R. Echenique [Argentine] ; HONGJUN CHEN [États-Unis] ; Troy Sutton [États-Unis] ; Daniel R. Perez [États-Unis]

Source :

RBID : Pascal:12-0142239

Descripteurs français

English descriptors

Abstract

We investigated the synergism between influenza virus and Streptococcus pneumoniae, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of S. pneumoniae to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential S. pneumoniae infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with S. pneumoniae. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.
pA  
A01 01  1    @0 0022-538X
A03   1    @0 J. virol.
A05       @2 86
A06       @2 7
A08 01  1  ENG  @1 Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia
A11 01  1    @1 CHOCKALINGAM (Ashok K.)
A11 02  1    @1 HICKMAN (Danielle)
A11 03  1    @1 PENA (Lindomar)
A11 04  1    @1 JIANQIANG YE
A11 05  1    @1 FERRERO (Andrea)
A11 06  1    @1 ECHENIQUE (Jose R.)
A11 07  1    @1 HONGJUN CHEN
A11 08  1    @1 SUTTON (Troy)
A11 09  1    @1 PEREZ (Daniel R.)
A14 01      @1 Department of Veterinary Medicine, University of Maryland @2 College Park, Maryland @3 USA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 7 aut. @Z 8 aut. @Z 9 aut.
A14 02      @1 Departamento de Bioquimica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Cordoba, Ciudad Universitaria @2 Córdoba @3 ARG @Z 6 aut.
A20       @1 3564-3573
A21       @1 2012
A23 01      @0 ENG
A43 01      @1 INIST @2 13592 @5 354000509213870150
A44       @0 0000 @1 © 2012 INIST-CNRS. All rights reserved.
A45       @0 38 ref.
A47 01  1    @0 12-0142239
A60       @1 P
A61       @0 A
A64 01  1    @0 Journal of virology
A66 01      @0 USA
C01 01    ENG  @0 We investigated the synergism between influenza virus and Streptococcus pneumoniae, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of S. pneumoniae to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential S. pneumoniae infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with S. pneumoniae. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.
C02 01  X    @0 002A05C10
C03 01  X  FRE  @0 Influenzavirus aviaire @2 NW @5 01
C03 01  X  ENG  @0 Avian influenzavirus @2 NW @5 01
C03 01  X  SPA  @0 Avian influenzavirus @2 NW @5 01
C03 02  X  FRE  @0 Délétion @5 05
C03 02  X  ENG  @0 Deletion @5 05
C03 02  X  SPA  @0 Deleción @5 05
C03 03  X  FRE  @0 Mutation @5 06
C03 03  X  ENG  @0 Mutation @5 06
C03 03  X  SPA  @0 Mutación @5 06
C03 04  X  FRE  @0 Soustype @5 07
C03 04  X  ENG  @0 Subtype @5 07
C03 04  X  SPA  @0 Subtipo @5 07
C03 05  X  FRE  @0 Pneumonie bactérienne @2 NM @5 14
C03 05  X  ENG  @0 Bacterial pneumonia @2 NM @5 14
C03 05  X  SPA  @0 Neumonía bacteriana @2 NM @5 14
C07 01  X  FRE  @0 Influenzavirus A @2 NW
C07 01  X  ENG  @0 Influenzavirus A @2 NW
C07 01  X  SPA  @0 Influenzavirus A @2 NW
C07 02  X  FRE  @0 Orthomyxoviridae @2 NW
C07 02  X  ENG  @0 Orthomyxoviridae @2 NW
C07 02  X  SPA  @0 Orthomyxoviridae @2 NW
C07 03  X  FRE  @0 Virus @2 NW
C07 03  X  ENG  @0 Virus @2 NW
C07 03  X  SPA  @0 Virus @2 NW
C07 04  X  FRE  @0 Pathologie de l'appareil respiratoire @5 13
C07 04  X  ENG  @0 Respiratory disease @5 13
C07 04  X  SPA  @0 Aparato respiratorio patología @5 13
C07 05  X  FRE  @0 Pathologie des poumons @5 16
C07 05  X  ENG  @0 Lung disease @5 16
C07 05  X  SPA  @0 Pulmón patología @5 16
N21       @1 107
N44 01      @1 OTO
N82       @1 OTO

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Pascal:12-0142239

Le document en format XML

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<term>Avian influenzavirus</term>
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<term>Deletion</term>
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<term>Influenzavirus aviaire</term>
<term>Délétion</term>
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<div type="abstract" xml:lang="en">We investigated the synergism between influenza virus and Streptococcus pneumoniae, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of S. pneumoniae to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential S. pneumoniae infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with S. pneumoniae. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.</div>
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<s1>JIANQIANG YE</s1>
</fA11>
<fA11 i1="05" i2="1">
<s1>FERRERO (Andrea)</s1>
</fA11>
<fA11 i1="06" i2="1">
<s1>ECHENIQUE (Jose R.)</s1>
</fA11>
<fA11 i1="07" i2="1">
<s1>HONGJUN CHEN</s1>
</fA11>
<fA11 i1="08" i2="1">
<s1>SUTTON (Troy)</s1>
</fA11>
<fA11 i1="09" i2="1">
<s1>PEREZ (Daniel R.)</s1>
</fA11>
<fA14 i1="01">
<s1>Department of Veterinary Medicine, University of Maryland</s1>
<s2>College Park, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Departamento de Bioquimica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Cordoba, Ciudad Universitaria</s1>
<s2>Córdoba</s2>
<s3>ARG</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20>
<s1>3564-3573</s1>
</fA20>
<fA21>
<s1>2012</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>13592</s2>
<s5>354000509213870150</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2012 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>38 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>12-0142239</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Journal of virology</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>We investigated the synergism between influenza virus and Streptococcus pneumoniae, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of S. pneumoniae to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential S. pneumoniae infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with S. pneumoniae. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002A05C10</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Influenzavirus aviaire</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Avian influenzavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Avian influenzavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Délétion</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Deletion</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Deleción</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Mutation</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Mutation</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Mutación</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Soustype</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Subtype</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Subtipo</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Pneumonie bactérienne</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Bacterial pneumonia</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Neumonía bacteriana</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Pathologie de l'appareil respiratoire</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Pathologie des poumons</s0>
<s5>16</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21>
<s1>107</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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   |wiki=    Sante
   |area=    H2N2V1
   |flux=    PascalFrancis
   |étape=   Curation
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   |clé=     Pascal:12-0142239
   |texte=   Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia
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