Nonlinkage of neurovirulence exclusively to viral hemagglutinin or neuraminidase in genetic recombinants of A-NWS (HON1) influenza virus.
Identifieur interne : 002C26 ( Main/Exploration ); précédent : 002C25; suivant : 002C27Nonlinkage of neurovirulence exclusively to viral hemagglutinin or neuraminidase in genetic recombinants of A-NWS (HON1) influenza virus.
Auteurs : V. Mayer ; J L Schulman ; E D KilbourneSource :
- Journal of virology [ 0022-538X ] ; 1973.
Descripteurs français
- KwdFr :
- Animaux, Cyclophosphamide (effets indésirables), Cyclophosphamide (pharmacologie), Embryon de poulet, Encéphale (microbiologie), Hybridation génétique, Hémagglutinines virales, Immunosuppresseurs (effets indésirables), Immunosuppresseurs (pharmacologie), Infections à Orthomyxoviridae (microbiologie), Infections à Orthomyxoviridae (mortalité), Infections à Orthomyxoviridae (traitement médicamenteux), Injections sous-cutanées, Mâle, Orthomyxoviridae (), Orthomyxoviridae (croissance et développement), Orthomyxoviridae (enzymologie), Orthomyxoviridae (immunologie), Orthomyxoviridae (pathogénicité), Recombinaison génétique, Réplication virale, Sialidase, Souris, Tests d'hémagglutination, Virulence.
- MESH :
- croissance et développement : Orthomyxoviridae.
- effets indésirables : Cyclophosphamide, Immunosuppresseurs.
- enzymologie : Orthomyxoviridae.
- immunologie : Orthomyxoviridae.
- microbiologie : Encéphale, Infections à Orthomyxoviridae.
- mortalité : Infections à Orthomyxoviridae.
- pathogénicité : Orthomyxoviridae.
- pharmacologie : Cyclophosphamide, Immunosuppresseurs.
- traitement médicamenteux : Infections à Orthomyxoviridae.
- Animaux, Embryon de poulet, Hybridation génétique, Hémagglutinines virales, Injections sous-cutanées, Mâle, Orthomyxoviridae, Recombinaison génétique, Réplication virale, Sialidase, Souris, Tests d'hémagglutination, Virulence.
English descriptors
- KwdEn :
- Animals, Brain (microbiology), Chick Embryo, Cyclophosphamide (adverse effects), Cyclophosphamide (pharmacology), Hemagglutination Tests, Hemagglutinins, Viral, Hybridization, Genetic, Immunosuppressive Agents (adverse effects), Immunosuppressive Agents (pharmacology), Injections, Subcutaneous, Male, Mice, Neuraminidase, Orthomyxoviridae (drug effects), Orthomyxoviridae (enzymology), Orthomyxoviridae (growth & development), Orthomyxoviridae (immunology), Orthomyxoviridae (pathogenicity), Orthomyxoviridae Infections (drug therapy), Orthomyxoviridae Infections (microbiology), Orthomyxoviridae Infections (mortality), Recombination, Genetic, Virulence, Virus Replication.
- MESH :
- chemical , adverse effects : Cyclophosphamide, Immunosuppressive Agents.
- drug effects : Orthomyxoviridae.
- drug therapy : Orthomyxoviridae Infections.
- enzymology : Orthomyxoviridae.
- growth & development : Orthomyxoviridae.
- immunology : Orthomyxoviridae.
- microbiology : Brain, Orthomyxoviridae Infections.
- mortality : Orthomyxoviridae Infections.
- pathogenicity : Orthomyxoviridae.
- chemical , pharmacology : Cyclophosphamide, Immunosuppressive Agents.
- Animals, Chick Embryo, Hemagglutination Tests, Hemagglutinins, Viral, Hybridization, Genetic, Injections, Subcutaneous, Male, Mice, Neuraminidase, Recombination, Genetic, Virulence, Virus Replication.
Abstract
Genetic recombination of the neurovirulent A/NWS/cc-p (H0N1) and the non-neurovirulent A/Jap.305/57 (H2N2) influenza viruses in which hemagglutinin and neuraminidase were segregated (H0N2, H2N1) were studied for neurovirulence in mice immunosuppressed with cyclophosphamide (CPA) which permitted full expression of virulence. Both H0N2 and H2N1 recombinants replicated in the brain (in contrast to the H2N2 parent) and both produced lethal effects in CPA-treated animals. Therefore we conclude that A/NWS (H0N1) neurovirulence is not exclusively linked with either the hemagglutinin or the neuraminidase of the virus. The H0N2 and H2N1 recombinants have revealed the existence of two separate attributes of neurovirulence: (i) the capacity of virus to initiate intracerebral infection and (ii) the capacity of infection, once initiated, to produce lethal disease. These studies provide further evidence for the polygenic nature of A/NWS neurovirulence.
PubMed: 4688703
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000663
- to stream PubMed, to step Curation: 000663
- to stream PubMed, to step Checkpoint: 000575
- to stream Ncbi, to step Merge: 001129
- to stream Ncbi, to step Curation: 001129
- to stream Ncbi, to step Checkpoint: 001129
- to stream Main, to step Merge: 002E01
- to stream Main, to step Curation: 002C26
Le document en format XML
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<term>Cyclophosphamide (pharmacologie)</term>
<term>Embryon de poulet</term>
<term>Encéphale (microbiologie)</term>
<term>Hybridation génétique</term>
<term>Hémagglutinines virales</term>
<term>Immunosuppresseurs (effets indésirables)</term>
<term>Immunosuppresseurs (pharmacologie)</term>
<term>Infections à Orthomyxoviridae (microbiologie)</term>
<term>Infections à Orthomyxoviridae (mortalité)</term>
<term>Infections à Orthomyxoviridae (traitement médicamenteux)</term>
<term>Injections sous-cutanées</term>
<term>Mâle</term>
<term>Orthomyxoviridae ()</term>
<term>Orthomyxoviridae (croissance et développement)</term>
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<term>Orthomyxoviridae (immunologie)</term>
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<term>Orthomyxoviridae Infections</term>
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<front><div type="abstract" xml:lang="en">Genetic recombination of the neurovirulent A/NWS/cc-p (H0N1) and the non-neurovirulent A/Jap.305/57 (H2N2) influenza viruses in which hemagglutinin and neuraminidase were segregated (H0N2, H2N1) were studied for neurovirulence in mice immunosuppressed with cyclophosphamide (CPA) which permitted full expression of virulence. Both H0N2 and H2N1 recombinants replicated in the brain (in contrast to the H2N2 parent) and both produced lethal effects in CPA-treated animals. Therefore we conclude that A/NWS (H0N1) neurovirulence is not exclusively linked with either the hemagglutinin or the neuraminidase of the virus. The H0N2 and H2N1 recombinants have revealed the existence of two separate attributes of neurovirulence: (i) the capacity of virus to initiate intracerebral infection and (ii) the capacity of infection, once initiated, to produce lethal disease. These studies provide further evidence for the polygenic nature of A/NWS neurovirulence.</div>
</front>
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<name sortKey="Schulman, J L" sort="Schulman, J L" uniqKey="Schulman J" first="J L" last="Schulman">J L Schulman</name>
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