Abstract |
Secondary pneumonia caused by Staphylococcus aureus is reemerging as a primary cause of excess mortality associated with infection by the influenza A virus. We have investigated in vitro the cellular and molecular mechanisms underlying this synergism. Experimental data show a significant increase in the efficiency of internalisation of S. aureus into cultured pneumocytes during the early phases of viral infection, while a relevant increase in the efficiency of adhesion is evident only later during viral infection, suggesting that the 2 effects are based on different molecular mechanisms. Data reported in this paper show that S. aureus cells can bind the viral hemagglutinin (HA) and that this binding promotes enhanced bacterial internalisation by 2 mechanisms: binding to HA exposed at the surface of infected cells and binding to free extracellular virions, enabling internalisation at high efficiency also in cells that are not infected by the virus. The affinity of binding that involves S. aureus and HA was shown to be enhanced by the reducing extracellular environment that the virus can generate.
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Authors | Claudio Passariello, Lucia Nencioni, Rossella Sgarbanti, Danilo Ranieri, Maria Rosaria Torrisi, Sandro Ripa, Enrico Garaci, Anna Teresa Palamara |
Journal | International journal of medical microbiology : IJMM
(Int J Med Microbiol)
Vol. 301
Issue 2
Pg. 97-104
(Feb 2011)
ISSN: 1618-0607 [Electronic] Germany |
PMID | 20940105
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2010 Elsevier GmbH. All rights reserved. |
Chemical References |
- Hemagglutinin Glycoproteins, Influenza Virus
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Topics |
- Alveolar Epithelial Cells
(microbiology, virology)
- Bacterial Adhesion
- Cell Line
- Endocytosis
- Hemagglutinin Glycoproteins, Influenza Virus
(metabolism)
- Humans
- Influenza A Virus, H1N1 Subtype
(pathogenicity)
- Microbial Interactions
- Protein Binding
- Staphylococcus aureus
(pathogenicity)
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