Disruption of virus-host cell interactions and cell signaling pathways as an anti-viral approach against influenza virus infections
Identifieur interne : 002298 ( Main/Exploration ); précédent : 002297; suivant : 002299Disruption of virus-host cell interactions and cell signaling pathways as an anti-viral approach against influenza virus infections
Auteurs : Stephan Ludwig [Allemagne]Source :
- Biological Chemistry [ 1431-6730 ] ; 2011.
English descriptors
- Teeft :
- Acetylsalicylic acid, Active site, Agents chemother, Animal models, Antiviral, Available drugs, Avian, Binding site, Biol, Blocker, Cascade, Caspase, Caspase inhibitors, Cause pandemics, Cell biol, Cell culture, Cell microbiol, Cell surface, Cellular, Cellular binding partners, Cellular factors, Cellular function, Cellular proteins, Chem, Cistus, Cistus incanus, Clinical practice, Clinical trials, Current drugs, Current options, Cytokine, Cytokine burst, Droebner, Early phase, Ehrhardt, Future pandemic virus, Genome, Geranium sanguineum, Hayden, High percentage, Host cell, Host cells, Human viruses, Infection, Inhibitor, Inhibitory activity, Interaction blockers, Interferon, Kinase, Lippencott willams, Ludwig, Mazur, Membrane accumulation, Molecular mechanisms, Molecular virology, Mouse infection model, Mouse model, Natural products, Neuraminidase, Neuraminidase inhibitors, Novel approach, Novel concept, Novel drugs, Novel inhibitor, Nuclear retention, Oseltamivir, Pandemic, Paradigm change, Pathogen, Pathway, Peptide, Pharmaceutical companies, Plant extracts, Planz, Pleschka, Plos pathog, Polymerase, Polymerase activity, Polyphenols, Preclinical development, Progeny virus titers, Protease, Protease inhibitors, Protein kinase, Proteolytic activation, Reading frame, Recent studies, Recent years, Receptor, Replication, Replication cycle, Resistant mutants, Resistant variants, Resistant virus variants, Respiratory epithelium, Resveratrol, Schmolke, Secondary pneumococcal infection, Several inhibitors, Side effects, Signal transduction, Suitable target, Toxic side effects, Traditional medicine, Transcription factor, Ubiquitin ligase, Vanden berghe, Viral, Viral attachment, Viral genome, Viral polymerase, Viral polymerase activity, Viral proteins, Viral replication, Viral resistance, Virion, Virol, Virology, Virus, Virus activity, Virus infection, Virus infections, Virus life cycle, Virus propagation, Virus protein, Virus replication, Virus titers, Wurzer.
Abstract
Influenza is still one of the major plagues worldwide with the threatening potential to cause pandemics. In recent years, increasing levels of resistance to the four FDA approved anti-influenza virus drugs have been described. This situation underlines the urgent need for novel anti-virals in preparation for future influenza epidemics or pandemics. Although the anti-virals currently in use target viral factors such as the neuraminidase or the M2 ion channel, there is an increase in pre-clinical approaches that focus on cellular factors or pathways that directly or indirectly interact with virus replication. This does not only include inhibitors of virus-supportive signaling cascades but also interaction blockers of viral proteins with host cell proteins. This review aims to highlight some of these novel approaches that represent a paradigm change in anti-viral strategies against the influenza virus. Although most of these approaches are still in an early phase of preclinical development they might be very promising particularly with respect to the prevention of viral resistance to potential drugs.
Url:
DOI: 10.1515/bc.2011.121
Affiliations:
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sanguineum</term><term>Hayden</term><term>High percentage</term><term>Host cell</term><term>Host cells</term><term>Human viruses</term><term>Infection</term><term>Inhibitor</term><term>Inhibitory activity</term><term>Interaction blockers</term><term>Interferon</term><term>Kinase</term><term>Lippencott willams</term><term>Ludwig</term><term>Mazur</term><term>Membrane accumulation</term><term>Molecular mechanisms</term><term>Molecular virology</term><term>Mouse infection model</term><term>Mouse model</term><term>Natural products</term><term>Neuraminidase</term><term>Neuraminidase inhibitors</term><term>Novel approach</term><term>Novel concept</term><term>Novel drugs</term><term>Novel inhibitor</term><term>Nuclear retention</term><term>Oseltamivir</term><term>Pandemic</term><term>Paradigm change</term><term>Pathogen</term><term>Pathway</term><term>Peptide</term><term>Pharmaceutical companies</term><term>Plant extracts</term><term>Planz</term><term>Pleschka</term><term>Plos 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In recent years, increasing levels of resistance to the four FDA approved anti-influenza virus drugs have been described. This situation underlines the urgent need for novel anti-virals in preparation for future influenza epidemics or pandemics. Although the anti-virals currently in use target viral factors such as the neuraminidase or the M2 ion channel, there is an increase in pre-clinical approaches that focus on cellular factors or pathways that directly or indirectly interact with virus replication. This does not only include inhibitors of virus-supportive signaling cascades but also interaction blockers of viral proteins with host cell proteins. This review aims to highlight some of these novel approaches that represent a paradigm change in anti-viral strategies against the influenza virus. Although most of these approaches are still in an early phase of preclinical development they might be very promising particularly with respect to the prevention of viral resistance to potential drugs.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>District de Münster</li><li>Rhénanie-du-Nord-Westphalie</li></region><settlement><li>Münster</li></settlement></list><tree><country name="Allemagne"><region name="Rhénanie-du-Nord-Westphalie"><name sortKey="Ludwig, Stephan" sort="Ludwig, Stephan" uniqKey="Ludwig S" first="Stephan" last="Ludwig">Stephan Ludwig</name></region><name sortKey="Ludwig, Stephan" sort="Ludwig, Stephan" uniqKey="Ludwig S" first="Stephan" last="Ludwig">Stephan Ludwig</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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