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Summary of a Meeting on the Origin of Pandemic Influenza Viruses

Identifieur interne : 002622 ( Main/Merge ); précédent : 002621; suivant : 002623

Summary of a Meeting on the Origin of Pandemic Influenza Viruses

Auteurs : W. Graeme Laver [République populaire de Chine] ; Robert G. Webster [République populaire de Chine] ; C. M. Chu [République populaire de Chine]

Source :

RBID : ISTEX:6B3E9D232A2EBEC8D9865366253F66076B48349E

Descripteurs français

English descriptors

Abstract

Influenza type A virus periodically undergoes major antigenic shifts in which the hemagglutinin (HAG) and sometimes the neuraminidase (NA) antigens are replaced by HAG and NA antigens of another subtype. Three such shifts have taken place since the virus was first isolated, and all appear to have occurred in China. The way in which these “new” influenza type A viruses suddenly appear (or reappear) in the human population is not known. At a meeting held in Beijing, China, on November 10–12, 1982, participants discussed the latest findings on the molecular biology of influenza viruses and on aspects of their ecology that may offer insight into the factors responsible for the origin of pandemic influenza viruses. Information obtained in earlier studies has provided some clues about how the antigenic shifts may occur. For example, the H3N2 virus has been found to be a recombinant deriving seven of its eight genes from an H2N2 strain and gene 4 (which encodes for the HAG) from some other virus, possibly an avian influenza virus of the H3 subtype [1–3]. In addition, studies of the genome of the HINI virus that appeared in Anshan, China, in 1977 have shown that this virus almost certainly underwent no replication for 27 years. This finding suggests that the virus existed in an animal reservoir during this period [4, 5].

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DOI: 10.1093/infdis/149.1.108

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ISTEX:6B3E9D232A2EBEC8D9865366253F66076B48349E

Le document en format XML

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</keywords>
<keywords scheme="MESH" type="geographic" xml:lang="en">
<term>China</term>
<term>Macromolecular Substances</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Influenza A virus</term>
<term>Orthomyxoviridae</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Orthomyxoviridae</term>
<term>Sialidase</term>
<term>Virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr">
<term>Antigènes viraux</term>
<term>Hémagglutinines virales</term>
<term>Lymphocytes T cytotoxiques</term>
<term>Orthomyxoviridae</term>
<term>Sialidase</term>
<term>Vaccins antigrippaux</term>
<term>Épitopes</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en">
<term>Orthomyxoviridae</term>
<term>T-Lymphocytes, Cytotoxic</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr">
<term>Grippe humaine</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en">
<term>Influenza, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr">
<term>Orthomyxoviridae</term>
<term>Virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en">
<term>Influenza A virus</term>
<term>Orthomyxoviridae</term>
</keywords>
<keywords scheme="MESH" qualifier="therapy" xml:lang="en">
<term>Influenza, Human</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Animals</term>
<term>Disease Reservoirs</term>
<term>Ecology</term>
<term>Genes, Viral</term>
<term>Humans</term>
<term>Recombination, Genetic</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>Animaux</term>
<term>Chine</term>
<term>Grippe humaine</term>
<term>Gènes viraux</term>
<term>Humains</term>
<term>Recombinaison génétique</term>
<term>Réplication virale</term>
<term>Réservoirs d'agents pathogènes</term>
<term>Structures macromoléculaires</term>
<term>Écologie</term>
</keywords>
<keywords scheme="Wicri" type="geographic" xml:lang="fr">
<term>République populaire de Chine</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Influenza type A virus periodically undergoes major antigenic shifts in which the hemagglutinin (HAG) and sometimes the neuraminidase (NA) antigens are replaced by HAG and NA antigens of another subtype. Three such shifts have taken place since the virus was first isolated, and all appear to have occurred in China. The way in which these "new" influenza type A viruses suddenly appear (or reappear) in the human population is not known. At a meeting held in Beijing, China, on November 10-12, 1982, participants discussed the latest findings on the molecular biology of influenza viruses and on aspects of their ecology that may offer insight into the factors responsible for the origin of pandemic influenza viruses. Information obtained in earlier studies has provided some clues about how the antigenic shifts may occur. For example, the H3N2 virus has been found to be a recombinant deriving seven of its eight genes from an H2N2 strain and gene 4 (which encodes for the HAG) from some other virus, possibly an avian influenza virus of the H3 subtype [1-3]. In addition, studies of the genome of the H1N1 virus that appeared in Anshan, China, in 1977 have shown that this virus almost certainly underwent no replication for 27 years. This finding suggests that the virus existed in an animal reservoir during this period [4, 5].</div>
</front>
</TEI>
</PubMed>
</double>
</record>

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