H2N2V1, 1968, Analysis, bibRecord, 000150

Changes in H3 influenza A virus receptor specificity during replication in humans

Identifieur interne : 000150 ( 1968/Analysis ); précédent : 000149; suivant : 000151

Changes in H3 influenza A virus receptor specificity during replication in humans

Auteurs : Kathleen Ryan-Poirier [États-Unis] ; Yasuo Suzuki [Japon] ; William J. Bean [États-Unis] ; Darwyn Kobasa [États-Unis] ; Ayato Takada [États-Unis] ; Toshihiro Ito [Japon] ; Yoshihiro Kawaoka [États-Unis]

Source :

Virus Research [ 0168-1702 ] ; 1998.

RBID : ISTEX:87A95EBC891DB1FF395035DF4A195C20706CD65C

English descriptors

Teeft :
- Amino, Amino acid changes, Assay, Avian, Avian virus, Binding activity, Binding assay, Chain type, Chicken erythrocytes, Distinct glycoprotein inhibitors, Elsevier science, Gangliosides, Hemagglutination inhibition, Hemagglutinin, Horse serum, Host species, Human population, Human viruses, Infectious diseases, Inhibitor, Jude research hospital, Kawaoka, Linkage, Neutralization, Other viruses, Paulson, Potential glycosylation site, Present address, Rabbit sera, Receptor, Receptor binding, Receptor changes, Receptor determinants, Respiratory epithelium, Room temperature, Serum inhibitor sensitivity, Serum inhibitors, Serum sensitivity, Sialic, Sialic acid, Suzuki, Veterinary medicine, Viral infectivity, Virol, Virology, Virus, Virus binding, Virus hemagglutinin, Virus infection, Virus receptor, Virus research.

Abstract

Abstract: Influenza A viruses of the H3 subtype caused the 1968 Hong Kong pandemic, the hemagglutinin (HA) gene being introduced into humans following a reassortment event with an avian virus. Receptor specificity and serum inhibitor sensitivity of the HA of influenza A viruses are linked to the host species. Human H3 viruses preferentially recognize N-acetyl sialic acid linked to galactose by α2,6 linkages (Neu5Acα2,6Gal) and are sensitive to serum inhibitors, whereas avian and equine viruses preferentially recognize Neu5Acα2,3Gal linkages and are resistant to serum inhibitors. We have examined the receptor specificity and serum inhibitor sensitivity of H3 human influenza A viruses from the time they were introduced into the human population to gain insight into the mechanism of viral molecular evolution and host tropism. All of the viruses were sensitive to neutralization and hemagglutination inhibition by horse serum. Early H3 viruses were resistant to pig and rabbit serum inhibitors. Viruses isolated after 1977 were uniformly sensitive to inhibition by pig and rabbit sera. The recognition of Neu5Acα2,3Gal or Neu5Acα2,6Gal linkages was not correlated with the serum sensitivity. These data showed that the receptor specificity of HA, measured as inhibitor sensitivity, has changed during replication in humans since its introduction from an avian virus.

Url:

https://api.istex.fr/ark:/67375/6H6-FX44HDX4-K/fulltext.pdf

DOI: 10.1016/S0168-1702(98)00067-7

Affiliations:

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Links to Exploration step

ISTEX:87A95EBC891DB1FF395035DF4A195C20706CD65C

Le document en format XML

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<term>Infectious diseases</term>
<term>Inhibitor</term>
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<front><div type="abstract" xml:lang="en">Abstract: Influenza A viruses of the H3 subtype caused the 1968 Hong Kong pandemic, the hemagglutinin (HA) gene being introduced into humans following a reassortment event with an avian virus. Receptor specificity and serum inhibitor sensitivity of the HA of influenza A viruses are linked to the host species. Human H3 viruses preferentially recognize N-acetyl sialic acid linked to galactose by α2,6 linkages (Neu5Acα2,6Gal) and are sensitive to serum inhibitors, whereas avian and equine viruses preferentially recognize Neu5Acα2,3Gal linkages and are resistant to serum inhibitors. We have examined the receptor specificity and serum inhibitor sensitivity of H3 human influenza A viruses from the time they were introduced into the human population to gain insight into the mechanism of viral molecular evolution and host tropism. All of the viruses were sensitive to neutralization and hemagglutination inhibition by horse serum. Early H3 viruses were resistant to pig and rabbit serum inhibitors. Viruses isolated after 1977 were uniformly sensitive to inhibition by pig and rabbit sera. The recognition of Neu5Acα2,3Gal or Neu5Acα2,6Gal linkages was not correlated with the serum sensitivity. These data showed that the receptor specificity of HA, measured as inhibitor sensitivity, has changed during replication in humans since its introduction from an avian virus.</div>
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Changes in H3 influenza A virus receptor specificity during replication in humans

Changes in H3 influenza A virus receptor specificity during replication in humans

Source :

English descriptors

Abstract

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