Abstract
Influenza A virus remains a major public health problem. Mouse models have been widely used to study influenza infection in mammals. DBA/2J and C57BL/6J represent extremes in terms of susceptibility to influenza A infection among inbred laboratory mouse strains. Several studies focused specifically on the factors responsible for the susceptibility of DBA/2J or the resistance of C57BL/6J and resulted in impressive lists of candidate genes or factors over- or underexpressed in one of the strains. We adopted a different phenotypical approach to identify the critical steps of the infection process accounting for the differences between DBA/2J and C57BL/6J strains. We concluded that both a dysfunction of alveolar macrophages and an increased permissivity of respiratory cells rendered DBA/2J more susceptible to influenza infection.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alveolar Epithelial Cells / immunology*
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Alveolar Epithelial Cells / metabolism
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Alveolar Epithelial Cells / virology
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Animals
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Chemokines / genetics
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Chemokines / metabolism
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Complement System Proteins / immunology
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Cytokines / genetics
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Cytokines / metabolism
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Disease Models, Animal
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Disease Resistance
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Disease Susceptibility
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Gene Expression
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Immunohistochemistry
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Influenza A Virus, H1N1 Subtype / immunology
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Influenza A virus / immunology*
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Lung / immunology
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Lung / metabolism
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Lung / pathology
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Lung / virology
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Macrophages, Alveolar / immunology*
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Macrophages, Alveolar / metabolism
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Macrophages, Alveolar / virology
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Mice
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Mice, Inbred DBA
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N-Acetylneuraminic Acid / metabolism
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Orthomyxoviridae Infections / immunology*
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Orthomyxoviridae Infections / mortality
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Orthomyxoviridae Infections / pathology
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Orthomyxoviridae Infections / virology
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Respiratory Mucosa / immunology
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Respiratory Mucosa / metabolism
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Respiratory Mucosa / pathology
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Respiratory Mucosa / virology
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Viral Load
Substances
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Chemokines
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Cytokines
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Complement System Proteins
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N-Acetylneuraminic Acid