Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia
Identifieur interne : 000007 ( PascalFrancis/Corpus ); précédent : 000006; suivant : 000008Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia
Auteurs : Ashok K. Chockalingam ; Danielle Hickman ; Lindomar Pena ; JIANQIANG YE ; Andrea Ferrero ; Jose R. Echenique ; HONGJUN CHEN ; Troy Sutton ; Daniel R. PerezSource :
- Journal of virology [ 0022-538X ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Format Inist (serveur)
NO : | PASCAL 12-0142239 INIST |
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ET : | Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia |
AU : | CHOCKALINGAM (Ashok K.); HICKMAN (Danielle); PENA (Lindomar); JIANQIANG YE; FERRERO (Andrea); ECHENIQUE (Jose R.); HONGJUN CHEN; SUTTON (Troy); PEREZ (Daniel R.) |
AF : | Department of Veterinary Medicine, University of Maryland/College Park, Maryland/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 7 aut., 8 aut., 9 aut.); Departamento de Bioquimica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Cordoba, Ciudad Universitaria/Córdoba/Argentine (6 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2012; Vol. 86; No. 7; Pp. 3564-3573; Bibl. 38 ref. |
LA : | Anglais |
EA : | 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. |
CC : | 002A05C10 |
FD : | Influenzavirus aviaire; Délétion; Mutation; Soustype; Pneumonie bactérienne |
FG : | Influenzavirus A; Orthomyxoviridae; Virus; Pathologie de l'appareil respiratoire; Pathologie des poumons |
ED : | Avian influenzavirus; Deletion; Mutation; Subtype; Bacterial pneumonia |
EG : | Influenzavirus A; Orthomyxoviridae; Virus; Respiratory disease; Lung disease |
SD : | Avian influenzavirus; Deleción; Mutación; Subtipo; Neumonía bacteriana |
LO : | INIST-13592.354000509213870150 |
ID : | 12-0142239 |
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Pascal:12-0142239Le document en format XML
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<front><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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<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>
<server><NO>PASCAL 12-0142239 INIST</NO>
<ET>Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia</ET>
<AU>CHOCKALINGAM (Ashok K.); HICKMAN (Danielle); PENA (Lindomar); JIANQIANG YE; FERRERO (Andrea); ECHENIQUE (Jose R.); HONGJUN CHEN; SUTTON (Troy); PEREZ (Daniel R.)</AU>
<AF>Department of Veterinary Medicine, University of Maryland/College Park, Maryland/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 7 aut., 8 aut., 9 aut.); Departamento de Bioquimica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Cordoba, Ciudad Universitaria/Córdoba/Argentine (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2012; Vol. 86; No. 7; Pp. 3564-3573; Bibl. 38 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002A05C10</CC>
<FD>Influenzavirus aviaire; Délétion; Mutation; Soustype; Pneumonie bactérienne</FD>
<FG>Influenzavirus A; Orthomyxoviridae; Virus; Pathologie de l'appareil respiratoire; Pathologie des poumons</FG>
<ED>Avian influenzavirus; Deletion; Mutation; Subtype; Bacterial pneumonia</ED>
<EG>Influenzavirus A; Orthomyxoviridae; Virus; Respiratory disease; Lung disease</EG>
<SD>Avian influenzavirus; Deleción; Mutación; Subtipo; Neumonía bacteriana</SD>
<LO>INIST-13592.354000509213870150</LO>
<ID>12-0142239</ID>
</server>
</inist>
</record>
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