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Evaluation of A/Alaska/6/77 (H3N2) cold-adapted recombinant viruses derived from A/Ann Arbor/6/60 cold-adapted donor virus in adult seronegative volunteers.

Identifieur interne : 002706 ( Main/Exploration ); précédent : 002705; suivant : 002707

Evaluation of A/Alaska/6/77 (H3N2) cold-adapted recombinant viruses derived from A/Ann Arbor/6/60 cold-adapted donor virus in adult seronegative volunteers.

Auteurs : B R Murphy ; R M Chanock ; M L Clements ; W C Anthony ; A J Sear ; L A Cisneros ; M B Rennels ; E H Miller ; R E Black ; M M Levine ; R F Betts ; R G Douglas ; H F Maassab ; N J Cox ; A P Kendal

Source :

RBID : pubmed:7251144

Descripteurs français

English descriptors

Abstract

The influenza A/Ann Arbor/6/60 (H2N2) cold-adapted (ca) virus was evaluated as a donor of attenuating genes to new variants of influenza A virus. This ca donor virus was mated with the A/Alaska/6/77 (H3N2) wild-type virus, and three A/Alaska/6/77 (H3N2) ca recombinant viruses were produced. The parental origin of the genes in the three ca recombinants had been determined previously (2), and their virulence for adult seronegative volunteers was assessed in the present study to identify the genes present in the ca donor virus that confer attenuation. Each of the recombinants received the hemagglutinin and neuraminidase genes from the A/Alaska/6/77 (H3N2) wild-type parent. One ca recombinant (CR-29) received all six transferable genes from the ca parent and was found to be satisfactorily attenuated in the volunteers. The two other ca recombinants received five of the six transferable genes with a wild-type gene at the M or NS locus. The pattern of infection in humans with these latter two ca recombinants was similar to the CR-29 ca recombinant. These findings demonstrate that inheritance of a gene in ca recombinants at the M or NS locus segregates independently of attenuation and suggest that the M and NS genes present in the ca donor virus are not the major determinants of attenuation conferred by this virus.

PubMed: 7251144


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Le document en format XML

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<term>Hemagglutinins, Viral (genetics)</term>
<term>Humans</term>
<term>Influenza A Virus, H3N2 Subtype</term>
<term>Influenza A virus (genetics)</term>
<term>Influenza A virus (immunology)</term>
<term>Influenza A virus (pathogenicity)</term>
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<term>Recombination, Genetic</term>
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<term>Anticorps antiviraux (biosynthèse)</term>
<term>Basse température</term>
<term>Gènes viraux</term>
<term>Humains</term>
<term>Hémagglutinines virales (génétique)</term>
<term>Recombinaison génétique</term>
<term>Sialidase (génétique)</term>
<term>Sous-type H3N2 du virus de la grippe A</term>
<term>Virus de la grippe A (génétique)</term>
<term>Virus de la grippe A (immunologie)</term>
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<div type="abstract" xml:lang="en">The influenza A/Ann Arbor/6/60 (H2N2) cold-adapted (ca) virus was evaluated as a donor of attenuating genes to new variants of influenza A virus. This ca donor virus was mated with the A/Alaska/6/77 (H3N2) wild-type virus, and three A/Alaska/6/77 (H3N2) ca recombinant viruses were produced. The parental origin of the genes in the three ca recombinants had been determined previously (2), and their virulence for adult seronegative volunteers was assessed in the present study to identify the genes present in the ca donor virus that confer attenuation. Each of the recombinants received the hemagglutinin and neuraminidase genes from the A/Alaska/6/77 (H3N2) wild-type parent. One ca recombinant (CR-29) received all six transferable genes from the ca parent and was found to be satisfactorily attenuated in the volunteers. The two other ca recombinants received five of the six transferable genes with a wild-type gene at the M or NS locus. The pattern of infection in humans with these latter two ca recombinants was similar to the CR-29 ca recombinant. These findings demonstrate that inheritance of a gene in ca recombinants at the M or NS locus segregates independently of attenuation and suggest that the M and NS genes present in the ca donor virus are not the major determinants of attenuation conferred by this virus.</div>
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