The pathogenesis of influenza in humans
Identifieur interne : 001856 ( Main/Exploration ); précédent : 001855; suivant : 001857The pathogenesis of influenza in humans
Auteurs : Maria C. Zambon [Royaume-Uni]Source :
- Reviews in Medical Virology [ 1052-9276 ] ; 2001-07.
English descriptors
- Teeft :
- Acad, Active site, Amino, Amino acid substitutions, Amino acids, Animal reservoir, Annual epidemics, Antigenic drift, Aquatic birds, Avian, Avian strains, Avian tissue, Avian virus, Avian viruses, Bacterial proteases, Carbohydrate moiety, Central role, Cleavage, Cleavage activation, Cleavage sequence, Cleavage sequences, Cleavage site, Cleavage sites, Copyright, Cytokine, Cytokine production, Determinant, Different viruses, Direct evidence, Direct transmission, Domestic poultry, Epithelial cells, Equine viruses, Fusion glycoprotein, Gastrointestinal tract, Gene, Gene encoding, Genetic analysis, Genome, Glycoprotein, Greater adaptation, Hemagglutinin, Homopolymeric sequences, Hong kong, Host cell, Host cells, Host factors, Host proteases, Host range, Human disease, Human host, Human transmission, Human virus, Human viruses, Infection, Initial mutation, Internal organs, Intranasal inoculation, John wiley sons, Kawaoka, Lysine, Lysine residue, Mammal, Mammalian host, Mouse model, Multibasic cleavage site, Mutation, Natl, Natural reservoir, Neuraminidase, Nucleotide, Nucleotide sequence, Other factors, Other genes, Outbreak, Pandemic, Pandemic strain, Pandemic viruses, Pathogenesis, Pathogenic, Pathogenic strains, Pathogenic viruses, Pathogenicity, Plasminogen, Plasminogen sequestration, Polybasic, Polymerase, Polymerase proteins, Proc, Proc natl acad, Protease, Proteolytic cleavage, Public health laboratory, Rapid evolution, Reassortant viruses, Recent work, Receptor, Receptor binding properties, Receptor binding site, Receptor preference, Replication, Replication cycle, Replication errors, Respiratory epithelium, Respiratory illness, Respiratory tract, Respiratory virus laboratory, Rkrk motif, Serine proteases, Sialic, Sialic acid, Steric hindrance, Structural elements, Subsequent insertion, Subtypes, Surface glycoproteins, Systemic, Systemic features, Systemic illness, Systemic infection, Systemic replication, Systemic spread, Systemic symptoms, Tissue tropism, Tropism, Viral, Viral polypeptides, Viral replication, Viral subtypes, Virol, Virology, Virus, Virus genes, Virus genome, Virus haemagglutinin, Virus hemagglutinin, Virus pathogenicity, Wild birds, Zambon.
Abstract
The rapid evolution of influenza A and B viruses contributes to annual influenza epidemics in humans. In addition, pandemics of influenza are also caused by influenza A viruses, whereas influenza B does not have the potential to cause pandemics because there is no animal reservoir of the virus. Study of the genetic differences between influenza A and influenza B viruses, which are restricted to humans, may be informative in understanding the factors that govern mammalian adaptation of influenza A viruses. Aquatic birds provide the natural reservoir for influenza A viruses, but in general, avian influenza is asymptomatic in feral birds. Occasionally, however, highly pathogenic strains of influenza cause serious systemic infections in domestic poultry. The pathogenicity of these strains is related to the presence of a polybasic cleavage sequence in the precursor of the surface glycoprotein haemagglutinin, which makes the glycoprotein susceptible to activation by ubiquitous proteases such as furin and PC6. However, the mechanism of pathogenicity may differ in highly pathogenic strains of human influenza, such as the H1N1 pandemic strain of 1918 and the H5N1 strain involved in the outbreak in Hong Kong in 1997. Binding of host proteases by the viral neuraminidase to assist activation of the haemagglutinin, shortening of the neuraminidase and substitutions in the polymerase gene, PB2, have all been suggested as alternative molecular correlates of pathogenicity of human influenza viruses. Additionally, systemic spread in humans of pathogenic subtypes has not been demonstrated and host factors such as interferons may be crucial in preventing the spread of the virus outside the respiratory tract. Copyright © 2001 John Wiley & Sons, Ltd.
Url:
DOI: 10.1002/rmv.319
Affiliations:
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Le document en format XML
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<term>Annual epidemics</term>
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<term>Avian tissue</term>
<term>Avian virus</term>
<term>Avian viruses</term>
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<term>Carbohydrate moiety</term>
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<term>Cleavage sequence</term>
<term>Cleavage sequences</term>
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<term>Cleavage sites</term>
<term>Copyright</term>
<term>Cytokine</term>
<term>Cytokine production</term>
<term>Determinant</term>
<term>Different viruses</term>
<term>Direct evidence</term>
<term>Direct transmission</term>
<term>Domestic poultry</term>
<term>Epithelial cells</term>
<term>Equine viruses</term>
<term>Fusion glycoprotein</term>
<term>Gastrointestinal tract</term>
<term>Gene</term>
<term>Gene encoding</term>
<term>Genetic analysis</term>
<term>Genome</term>
<term>Glycoprotein</term>
<term>Greater adaptation</term>
<term>Hemagglutinin</term>
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<front><div type="abstract" xml:lang="en">The rapid evolution of influenza A and B viruses contributes to annual influenza epidemics in humans. In addition, pandemics of influenza are also caused by influenza A viruses, whereas influenza B does not have the potential to cause pandemics because there is no animal reservoir of the virus. Study of the genetic differences between influenza A and influenza B viruses, which are restricted to humans, may be informative in understanding the factors that govern mammalian adaptation of influenza A viruses. Aquatic birds provide the natural reservoir for influenza A viruses, but in general, avian influenza is asymptomatic in feral birds. Occasionally, however, highly pathogenic strains of influenza cause serious systemic infections in domestic poultry. The pathogenicity of these strains is related to the presence of a polybasic cleavage sequence in the precursor of the surface glycoprotein haemagglutinin, which makes the glycoprotein susceptible to activation by ubiquitous proteases such as furin and PC6. However, the mechanism of pathogenicity may differ in highly pathogenic strains of human influenza, such as the H1N1 pandemic strain of 1918 and the H5N1 strain involved in the outbreak in Hong Kong in 1997. Binding of host proteases by the viral neuraminidase to assist activation of the haemagglutinin, shortening of the neuraminidase and substitutions in the polymerase gene, PB2, have all been suggested as alternative molecular correlates of pathogenicity of human influenza viruses. Additionally, systemic spread in humans of pathogenic subtypes has not been demonstrated and host factors such as interferons may be crucial in preventing the spread of the virus outside the respiratory tract. Copyright © 2001 John Wiley & Sons, Ltd.</div>
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