H2N2V1, PascalFrancis, Corpus, bibRecord, 000017

A 27-Amino-Acid Deletion in the Neuraminidase Stalk Supports Replication of an Avian H2N2 Influenza A Virus in the Respiratory Tract of Chickens

Identifieur interne : 000017 ( PascalFrancis/Corpus ); précédent : 000016; suivant : 000018

A 27-Amino-Acid Deletion in the Neuraminidase Stalk Supports Replication of an Avian H2N2 Influenza A Virus in the Respiratory Tract of Chickens

Auteurs : Erin M. Sorrell ; HAICHEN SONG ; Lindomar Pena ; Daniel R. Perez

Source :

Journal of virology [ 0022-538X ] ; 2010.

RBID : Pascal:10-0511482

Descripteurs français

Pascal (Inist)
- Influenzavirus aviaire, Virus grippal A, Poulet, Délétion, Mutation, Réplication, Voie respiratoire, Vétérinaire.

English descriptors

KwdEn :
- Avian influenzavirus, Chicken, Deletion, Influenza A virus, Mutation, Replication, Respiratory tract, Veterinary.

Abstract

The events and mechanisms that lead to interspecies transmission of, and host adaptation to, influenza A virus are unknown; however, both surface and internal proteins have been implicated. Our previous report highlighted the role that Japanese quail play as an intermediate host, expanding the host range of a mallard H2N2 virus, A/mallard/Potsdam/178-4/83 (H2N2), through viral adaptation. This quail-adapted virus supported transmission in quail and increased its host range to replicate and be transmitted efficiently in chickens. Here we report that of the six amino acid changes in the quail-adapted virus, a single change in the hemagglutinin (HA) was crucial for transmission in quail, while the changes in the polymerase genes favored replication at lower temperatures than those for the wild-type mallard virus. Reverse genetic analysis indicated that all adaptive mutations were necessary for transmission in chickens, further implicating quail in extending this virus to terrestrial poultry. Adaptation of the quail-adapted virus in chickens resulted in the alteration of viral tropism from intestinal shedding to shedding and transmission via the respiratory tract. Sequence analysis indicated that this chicken-adapted virus maintained all quail-adaptive mutations, as well as an additional change in the HA and, most notably, a 27-amino-acid deletion in the stalk region of neuraminidase (NA), a genotypic marker of influenza virus adaptation to chickens. This stalk deletion was shown to be responsible for the change in virus tropism from the intestine to the respiratory tract.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 The events and mechanisms that lead to interspecies transmission of, and host adaptation to, influenza A virus are unknown; however, both surface and internal proteins have been implicated. Our previous report highlighted the role that Japanese quail play as an intermediate host, expanding the host range of a mallard H2N2 virus, A/mallard/Potsdam/178-4/83 (H2N2), through viral adaptation. This quail-adapted virus supported transmission in quail and increased its host range to replicate and be transmitted efficiently in chickens. Here we report that of the six amino acid changes in the quail-adapted virus, a single change in the hemagglutinin (HA) was crucial for transmission in quail, while the changes in the polymerase genes favored replication at lower temperatures than those for the wild-type mallard virus. Reverse genetic analysis indicated that all adaptive mutations were necessary for transmission in chickens, further implicating quail in extending this virus to terrestrial poultry. Adaptation of the quail-adapted virus in chickens resulted in the alteration of viral tropism from intestinal shedding to shedding and transmission via the respiratory tract. Sequence analysis indicated that this chicken-adapted virus maintained all quail-adaptive mutations, as well as an additional change in the HA and, most notably, a 27-amino-acid deletion in the stalk region of neuraminidase (NA), a genotypic marker of influenza virus adaptation to chickens. This stalk deletion was shown to be responsible for the change in virus tropism from the intestine to the respiratory tract.
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C03	`01`	`X`	`ENG`	`@0 Avian influenzavirus @2 NW @5 01`
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C03	`04`	`X`	`ENG`	`@0 Deletion @5 05`
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C03	`05`	`X`	`FRE`	`@0 Mutation @5 06`
C03	`05`	`X`	`ENG`	`@0 Mutation @5 06`
C03	`05`	`X`	`SPA`	`@0 Mutación @5 06`
C03	`06`	`X`	`FRE`	`@0 Réplication @5 07`
C03	`06`	`X`	`ENG`	`@0 Replication @5 07`
C03	`06`	`X`	`SPA`	`@0 Replicación @5 07`
C03	`07`	`X`	`FRE`	`@0 Voie respiratoire @5 08`
C03	`07`	`X`	`ENG`	`@0 Respiratory tract @5 08`
C03	`07`	`X`	`SPA`	`@0 Vía respiratoria @5 08`
C03	`08`	`X`	`FRE`	`@0 Vétérinaire @5 45`
C03	`08`	`X`	`ENG`	`@0 Veterinary @5 45`
C03	`08`	`X`	`SPA`	`@0 Veterinario @5 45`
C07	`01`	`X`	`FRE`	`@0 Influenzavirus A @2 NW`
C07	`01`	`X`	`ENG`	`@0 Influenzavirus A @2 NW`
C07	`01`	`X`	`SPA`	`@0 Influenzavirus A @2 NW`
C07	`02`	`X`	`FRE`	`@0 Orthomyxoviridae @2 NW`
C07	`02`	`X`	`ENG`	`@0 Orthomyxoviridae @2 NW`
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C07	`04`	`X`	`FRE`	`@0 Aves @2 NS`
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C07	`05`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`05`	`X`	`ENG`	`@0 Vertebrata @2 NS`
C07	`05`	`X`	`SPA`	`@0 Vertebrata @2 NS`
N21				`@1 347`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 10-0511482 INIST
ET :	A 27-Amino-Acid Deletion in the Neuraminidase Stalk Supports Replication of an Avian H2N2 Influenza A Virus in the Respiratory Tract of Chickens
AU :	SORRELL (Erin M.); HAICHEN SONG; PENA (Lindomar); PEREZ (Daniel R.)
AF :	University of Maryland, College Park, Virginia-Maryland College of Veterinary Medicine/Etats-Unis (1 aut., 3 aut., 4 aut.); Department of Veterinary Medicine, and Synbiotics Corporation,8075 Greenmead Drive/College Park, Maryland 20742/Etats-Unis (2 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2010; Vol. 84; No. 22; Pp. 11831-11840; Bibl. 46 ref.
LA :	Anglais
EA :	The events and mechanisms that lead to interspecies transmission of, and host adaptation to, influenza A virus are unknown; however, both surface and internal proteins have been implicated. Our previous report highlighted the role that Japanese quail play as an intermediate host, expanding the host range of a mallard H2N2 virus, A/mallard/Potsdam/178-4/83 (H2N2), through viral adaptation. This quail-adapted virus supported transmission in quail and increased its host range to replicate and be transmitted efficiently in chickens. Here we report that of the six amino acid changes in the quail-adapted virus, a single change in the hemagglutinin (HA) was crucial for transmission in quail, while the changes in the polymerase genes favored replication at lower temperatures than those for the wild-type mallard virus. Reverse genetic analysis indicated that all adaptive mutations were necessary for transmission in chickens, further implicating quail in extending this virus to terrestrial poultry. Adaptation of the quail-adapted virus in chickens resulted in the alteration of viral tropism from intestinal shedding to shedding and transmission via the respiratory tract. Sequence analysis indicated that this chicken-adapted virus maintained all quail-adaptive mutations, as well as an additional change in the HA and, most notably, a 27-amino-acid deletion in the stalk region of neuraminidase (NA), a genotypic marker of influenza virus adaptation to chickens. This stalk deletion was shown to be responsible for the change in virus tropism from the intestine to the respiratory tract.
CC :	002A05C10
FD :	Influenzavirus aviaire; Virus grippal A; Poulet; Délétion; Mutation; Réplication; Voie respiratoire; Vétérinaire
FG :	Influenzavirus A; Orthomyxoviridae; Virus; Aves; Vertebrata
ED :	Avian influenzavirus; Influenza A virus; Chicken; Deletion; Mutation; Replication; Respiratory tract; Veterinary
EG :	Influenzavirus A; Orthomyxoviridae; Virus; Aves; Vertebrata
SD :	Avian influenzavirus; Influenza A virus; Pollo; Deleción; Mutación; Replicación; Vía respiratoria; Veterinario
LO :	INIST-13592.354000191376530220
ID :	10-0511482

Links to Exploration step

Pascal:10-0511482

Le document en format XML

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<front><div type="abstract" xml:lang="en">The events and mechanisms that lead to interspecies transmission of, and host adaptation to, influenza A virus are unknown; however, both surface and internal proteins have been implicated. Our previous report highlighted the role that Japanese quail play as an intermediate host, expanding the host range of a mallard H2N2 virus, A/mallard/Potsdam/178-4/83 (H2N2), through viral adaptation. This quail-adapted virus supported transmission in quail and increased its host range to replicate and be transmitted efficiently in chickens. Here we report that of the six amino acid changes in the quail-adapted virus, a single change in the hemagglutinin (HA) was crucial for transmission in quail, while the changes in the polymerase genes favored replication at lower temperatures than those for the wild-type mallard virus. Reverse genetic analysis indicated that all adaptive mutations were necessary for transmission in chickens, further implicating quail in extending this virus to terrestrial poultry. Adaptation of the quail-adapted virus in chickens resulted in the alteration of viral tropism from intestinal shedding to shedding and transmission via the respiratory tract. Sequence analysis indicated that this chicken-adapted virus maintained all quail-adaptive mutations, as well as an additional change in the HA and, most notably, a 27-amino-acid deletion in the stalk region of neuraminidase (NA), a genotypic marker of influenza virus adaptation to chickens. This stalk deletion was shown to be responsible for the change in virus tropism from the intestine to the respiratory tract.</div>
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<server><NO>PASCAL 10-0511482 INIST</NO>
<ET>A 27-Amino-Acid Deletion in the Neuraminidase Stalk Supports Replication of an Avian H2N2 Influenza A Virus in the Respiratory Tract of Chickens</ET>
<AU>SORRELL (Erin M.); HAICHEN SONG; PENA (Lindomar); PEREZ (Daniel R.)</AU>
<AF>University of Maryland, College Park, Virginia-Maryland College of Veterinary Medicine/Etats-Unis (1 aut., 3 aut., 4 aut.); Department of Veterinary Medicine, and Synbiotics Corporation,8075 Greenmead Drive/College Park, Maryland 20742/Etats-Unis (2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2010; Vol. 84; No. 22; Pp. 11831-11840; Bibl. 46 ref.</SO>
<LA>Anglais</LA>
<EA>The events and mechanisms that lead to interspecies transmission of, and host adaptation to, influenza A virus are unknown; however, both surface and internal proteins have been implicated. Our previous report highlighted the role that Japanese quail play as an intermediate host, expanding the host range of a mallard H2N2 virus, A/mallard/Potsdam/178-4/83 (H2N2), through viral adaptation. This quail-adapted virus supported transmission in quail and increased its host range to replicate and be transmitted efficiently in chickens. Here we report that of the six amino acid changes in the quail-adapted virus, a single change in the hemagglutinin (HA) was crucial for transmission in quail, while the changes in the polymerase genes favored replication at lower temperatures than those for the wild-type mallard virus. Reverse genetic analysis indicated that all adaptive mutations were necessary for transmission in chickens, further implicating quail in extending this virus to terrestrial poultry. Adaptation of the quail-adapted virus in chickens resulted in the alteration of viral tropism from intestinal shedding to shedding and transmission via the respiratory tract. Sequence analysis indicated that this chicken-adapted virus maintained all quail-adaptive mutations, as well as an additional change in the HA and, most notably, a 27-amino-acid deletion in the stalk region of neuraminidase (NA), a genotypic marker of influenza virus adaptation to chickens. This stalk deletion was shown to be responsible for the change in virus tropism from the intestine to the respiratory tract.</EA>
<CC>002A05C10</CC>
<FD>Influenzavirus aviaire; Virus grippal A; Poulet; Délétion; Mutation; Réplication; Voie respiratoire; Vétérinaire</FD>
<FG>Influenzavirus A; Orthomyxoviridae; Virus; Aves; Vertebrata</FG>
<ED>Avian influenzavirus; Influenza A virus; Chicken; Deletion; Mutation; Replication; Respiratory tract; Veterinary</ED>
<EG>Influenzavirus A; Orthomyxoviridae; Virus; Aves; Vertebrata</EG>
<SD>Avian influenzavirus; Influenza A virus; Pollo; Deleción; Mutación; Replicación; Vía respiratoria; Veterinario</SD>
<LO>INIST-13592.354000191376530220</LO>
<ID>10-0511482</ID>
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A 27-Amino-Acid Deletion in the Neuraminidase Stalk Supports Replication of an Avian H2N2 Influenza A Virus in the Respiratory Tract of Chickens

A 27-Amino-Acid Deletion in the Neuraminidase Stalk Supports Replication of an Avian H2N2 Influenza A Virus in the Respiratory Tract of Chickens

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