Caveolin-1 influences human influenza A virus (H1N1) multiplication in cell culture.
dc.contributor.author | Sun, Lijing | |
dc.contributor.author | Hemgård, Gun-Viol | |
dc.contributor.author | Susanto, Sony A | |
dc.contributor.author | Wirth, Manfred | |
dc.date.accessioned | 2016-01-14T12:21:25Z | en |
dc.date.available | 2016-01-14T12:21:25Z | en |
dc.date.issued | 2010 | en |
dc.identifier.citation | Caveolin-1 influences human influenza A virus (H1N1) multiplication in cell culture. 2010, 7:108 Virol. J. | en |
dc.identifier.issn | 1743-422X | en |
dc.identifier.pmid | 20504340 | en |
dc.identifier.doi | 10.1186/1743-422X-7-108 | en |
dc.identifier.uri | http://hdl.handle.net/10033/593391 | en |
dc.description.abstract | The threat of recurring influenza pandemics caused by new viral strains and the occurrence of escape mutants necessitate the search for potent therapeutic targets. The dependence of viruses on cellular factors provides a weak-spot in the viral multiplication strategy and a means to interfere with viral multiplication. | |
dc.language.iso | en | en |
dc.subject.mesh | Amino Acid Sequence | en |
dc.subject.mesh | Animals | en |
dc.subject.mesh | Caveolin 1 | en |
dc.subject.mesh | Cell Line | en |
dc.subject.mesh | Dogs | en |
dc.subject.mesh | Humans | en |
dc.subject.mesh | Influenza A Virus, H1N1 Subtype | en |
dc.subject.mesh | Influenza, Human | en |
dc.subject.mesh | Mice | en |
dc.subject.mesh | Molecular Sequence Data | en |
dc.subject.mesh | NIH 3T3 Cells | en |
dc.subject.mesh | Protein Binding | en |
dc.subject.mesh | Sequence Alignment | en |
dc.subject.mesh | Viral Matrix Proteins | en |
dc.subject.mesh | Virus Replication | en |
dc.title | Caveolin-1 influences human influenza A virus (H1N1) multiplication in cell culture. | en |
dc.type | Article | en |
dc.contributor.department | Helmholtz Centre for infection research, Inhoffenstr. 7, D-38124 Braunschweig, Germany. | en |
dc.identifier.journal | Virology journal | en |
refterms.dateFOA | 2018-06-12T23:37:13Z | |
html.description.abstract | The threat of recurring influenza pandemics caused by new viral strains and the occurrence of escape mutants necessitate the search for potent therapeutic targets. The dependence of viruses on cellular factors provides a weak-spot in the viral multiplication strategy and a means to interfere with viral multiplication. |