Influenza virus genetics
Identifieur interne : 001947 ( Main/Exploration ); précédent : 001946; suivant : 001948Influenza virus genetics
Auteurs : E. G. Brown [États-Unis]Source :
- Biomedicine & Pharmacotherapy [ 0753-3322 ] ; 2000.
English descriptors
- KwdEn :
- Teeft :
- Active site, Amantadine, Amino, Amino acid, Amino acid substitution, Amino acid substitutions, Amino acids, Amino terminal, Amino terminus, Analogue, Antigenic, Antigenic change, Antigenic shift, Antimicrob agents chemother, Avian, Avian strains, Avian viruses, Binding site, Block activation, Cause disease, Cell culture, Channel activity, Conformational change, Control virulence, Conventional genetics, Culture system, Different hosts, Drug sensitivity, Endosomal membrane, Enzyme inhibition, Fields virology, Foreign gene, Fusion peptide, Gene, Gene combination effects, Genealogical analysis, Genetic, Genetic analysis, Genetic control, Genetics, Genome, Genome segments, Guanidino group, Helper virus, Hemagglutinin, Host factors, Host restriction, Human infection, Human influenza viruses, Human population, Human strains, Human viruses, Immunocompromised child, Individual genes, Individual genome segments, Influenza, Influenza biology, Influenza disease, Influenza genes, Influenza genome, Influenza infection, Influenza strains, Influenza virus, Influenza virus nucleoprotein, Influenza viruses, Inhibitor, Interferon response, Localization, Matrix, Matrix protein, Mdck cells, Medicales elsevier, Membrane proteins, Mouse lung, Mouse model, Mrna, Mutant, Mutant genes, Mutant genome segment, Mutation, Neuraminidase, Neuraminidase inhibitors, Nuclear export, Nuclear import, Nuclear localization, Nuclear localization signal, Nuclear localization signals, Other genes, Palese, Parental, Parental origin, Parental strains, Phenotype, Plaque inhibition, Plasma membrane, Plenum press, Polymerase, Polymerase subunits, Primary structure, Proc nat1 acad, Progeny, Progeny virus, Protein, Protein kinase, Rational design, Reading frame, Reassortant viruses, Reassortants, Reassortment, Receptor, Receptor binding site, Receptor specificity, Replication, Resistant mutants, Resistant variants, Segmented genome, Selective pressure, Several studies, Sialic, Sialic acid, Side effects, Single subunit, Specific functions, Specific mutations, Substitution, Subunit, Subunit contacts, Suppressor mutations, Systemic effects, Variant, Viral, Viral assembly, Viral mrna, Virion, Virol, Virology, Virulence, Virulent, Virulent strains, Virulent variants, Virus, Virus genetics, Virus replication, Vrna, Zanamivir.
Abstract
Summary: Significant progress has been made in understanding the process of influenza A virus replication in cell culture; however, much less is known about the genetic control of virus-host interactions in disease. This review provides an overview of the genetic analysis of influenza virus biology. The functional map of the individual genes of influenza A virus is presented as well as the status of our current understanding of pathogenesis. Influenza has a segmented genome so it is possible to obtain reassortants that contain novel combinations of genome segments derived from different viruses. This is a very useful genetic tool and is also an important aspect of influenza evolution and biology. Human influenza viruses originate from avian strains of influenza virus so that influenza infection is at its basis a zoonosis. Influenza virus strains are host-restricted, however, and avian strains must be adapted to the human host. So questions of host-range and interaction with host factors are important determinants of the ability of influenza virus to cause disease in humans. Host-range is restricted primarily due to host-specific interactions of the ribonucleocapsid and the viral receptor. There are two classes of drugs for inhibiting influenza infection, amantadine HCl and neuraminidase inhibitors. The mode of action and basis for resistance to these drugs are presented. Prospective targets for antiviral therapy are also discussed.
Url:
DOI: 10.1016/S0753-3322(00)89026-5
Affiliations:
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virology</term><term>Foreign gene</term><term>Fusion peptide</term><term>Gene</term><term>Gene combination effects</term><term>Genealogical analysis</term><term>Genetic</term><term>Genetic analysis</term><term>Genetic control</term><term>Genetics</term><term>Genome</term><term>Genome segments</term><term>Guanidino group</term><term>Helper virus</term><term>Hemagglutinin</term><term>Host factors</term><term>Host restriction</term><term>Human infection</term><term>Human influenza viruses</term><term>Human population</term><term>Human strains</term><term>Human viruses</term><term>Immunocompromised child</term><term>Individual genes</term><term>Individual genome segments</term><term>Influenza</term><term>Influenza biology</term><term>Influenza disease</term><term>Influenza genes</term><term>Influenza genome</term><term>Influenza infection</term><term>Influenza strains</term><term>Influenza virus</term><term>Influenza virus nucleoprotein</term><term>Influenza viruses</term><term>Inhibitor</term><term>Interferon response</term><term>Localization</term><term>Matrix</term><term>Matrix protein</term><term>Mdck cells</term><term>Medicales elsevier</term><term>Membrane proteins</term><term>Mouse lung</term><term>Mouse model</term><term>Mrna</term><term>Mutant</term><term>Mutant genes</term><term>Mutant genome segment</term><term>Mutation</term><term>Neuraminidase</term><term>Neuraminidase inhibitors</term><term>Nuclear export</term><term>Nuclear import</term><term>Nuclear localization</term><term>Nuclear localization signal</term><term>Nuclear localization signals</term><term>Other genes</term><term>Palese</term><term>Parental</term><term>Parental origin</term><term>Parental strains</term><term>Phenotype</term><term>Plaque inhibition</term><term>Plasma membrane</term><term>Plenum press</term><term>Polymerase</term><term>Polymerase subunits</term><term>Primary structure</term><term>Proc nat1 acad</term><term>Progeny</term><term>Progeny virus</term><term>Protein</term><term>Protein kinase</term><term>Rational design</term><term>Reading frame</term><term>Reassortant viruses</term><term>Reassortants</term><term>Reassortment</term><term>Receptor</term><term>Receptor binding site</term><term>Receptor specificity</term><term>Replication</term><term>Resistant mutants</term><term>Resistant variants</term><term>Segmented genome</term><term>Selective pressure</term><term>Several studies</term><term>Sialic</term><term>Sialic acid</term><term>Side effects</term><term>Single subunit</term><term>Specific functions</term><term>Specific mutations</term><term>Substitution</term><term>Subunit</term><term>Subunit contacts</term><term>Suppressor mutations</term><term>Systemic effects</term><term>Variant</term><term>Viral</term><term>Viral assembly</term><term>Viral mrna</term><term>Virion</term><term>Virol</term><term>Virology</term><term>Virulence</term><term>Virulent</term><term>Virulent strains</term><term>Virulent 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This review provides an overview of the genetic analysis of influenza virus biology. The functional map of the individual genes of influenza A virus is presented as well as the status of our current understanding of pathogenesis. Influenza has a segmented genome so it is possible to obtain reassortants that contain novel combinations of genome segments derived from different viruses. This is a very useful genetic tool and is also an important aspect of influenza evolution and biology. Human influenza viruses originate from avian strains of influenza virus so that influenza infection is at its basis a zoonosis. Influenza virus strains are host-restricted, however, and avian strains must be adapted to the human host. So questions of host-range and interaction with host factors are important determinants of the ability of influenza virus to cause disease in humans. Host-range is restricted primarily due to host-specific interactions of the ribonucleocapsid and the viral receptor. There are two classes of drugs for inhibiting influenza infection, amantadine HCl and neuraminidase inhibitors. The mode of action and basis for resistance to these drugs are presented. Prospective targets for antiviral therapy are also discussed.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Brown, E G" sort="Brown, E G" uniqKey="Brown E" first="E. G." last="Brown">E. G. Brown</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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