H2N2V1, Ncbi, Curation, bibRecord, 000736

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

Identifieur interne : 000736 ( Ncbi/Curation ); précédent : 000735; suivant : 000737

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 :

Journal of Virology [ 0022-538X ] ; 2012.

RBID : PMC:3302490

Descripteurs français

English descriptors

KwdEn :
- Amino Acid Motifs, Animals, Bacterial Adhesion, Cell Line, Chickens, Coinfection (microbiology), Coinfection (virology), Female, Gene Deletion, Humans, Influenza A Virus, H2N2 Subtype (chemistry), Influenza A Virus, H2N2 Subtype (enzymology), Influenza A Virus, H2N2 Subtype (genetics), Influenza A Virus, H9N2 Subtype (chemistry), Influenza A Virus, H9N2 Subtype (enzymology), Influenza A Virus, H9N2 Subtype (genetics), Influenza in Birds (virology), Influenza, Human (complications), Influenza, Human (virology), Lung (microbiology), Lung (virology), Mice, Mice, Inbred BALB C, Neuraminidase (chemistry), Neuraminidase (genetics), Neuraminidase (metabolism), Pneumonia, Bacterial (complications), Pneumonia, Bacterial (microbiology), Streptococcus pneumoniae (physiology), Viral Proteins (chemistry), Viral Proteins (genetics), Viral Proteins (metabolism).
MESH :
- chemical , chemistry : Neuraminidase, Viral Proteins.
- chemistry : Influenza A Virus, H2N2 Subtype, Influenza A Virus, H9N2 Subtype.
- complications : Influenza, Human, Pneumonia, Bacterial.
- enzymology : Influenza A Virus, H2N2 Subtype, Influenza A Virus, H9N2 Subtype.
- genetics : Influenza A Virus, H2N2 Subtype, Influenza A Virus, H9N2 Subtype, Neuraminidase, Viral Proteins.
- chemical , metabolism : Neuraminidase, Viral Proteins.
- microbiology : Coinfection, Lung, Pneumonia, Bacterial.
- physiology : Streptococcus pneumoniae.
- virology : Coinfection, Influenza in Birds, Influenza, Human, Lung.
- Amino Acid Motifs, Animals, Bacterial Adhesion, Cell Line, Chickens, Female, Gene Deletion, Humans, Mice, Mice, Inbred BALB C.

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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302490

DOI: 10.1128/JVI.05809-11
PubMed: 22278240
PubMed Central: 3302490

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Le document en format XML

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<term>Bacterial Adhesion</term>
<term>Cell Line</term>
<term>Chickens</term>
<term>Female</term>
<term>Gene Deletion</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adhérence bactérienne</term>
<term>Animaux</term>
<term>Délétion de gène</term>
<term>Femelle</term>
<term>Grippe humaine</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Motifs d'acides aminés</term>
<term>Pneumopathie bactérienne</term>
<term>Poulets</term>
<term>Protéines virales</term>
<term>Sialidase</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Sous-type H2N2 du virus de la grippe A</term>
<term>Sous-type H9N2 du virus de la grippe A</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>We investigated the synergism between influenza virus and <named-content content-type="genus-species">Streptococcus pneumoniae</named-content>
, 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 <named-content content-type="genus-species">S. pneumoniae</named-content>
 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 <named-content content-type="genus-species">S. pneumoniae</named-content>
 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 <named-content content-type="genus-species">S. pneumoniae</named-content>
. 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.</p>
</div>
</front>
</TEI>
</record>

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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

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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