Experimental Myocarditis Induced in Mice by Infection with Influenza A2 Virus
Identifieur interne : 002761 ( Main/Exploration ); précédent : 002760; suivant : 002762Experimental Myocarditis Induced in Mice by Infection with Influenza A2 Virus
Auteurs : Masahiro Sakamoto ; Fujio Suzuki ; Sumio Arai ; Tamotsu Takishima ; Nakao IshidaSource :
- Microbiology and Immunology [ 0385-5600 ] ; 1981-02.
Descripteurs français
- KwdFr :
- Animaux, Coeur (microbiologie), Femelle, Infections à Orthomyxoviridae (), Modèles animaux de maladie humaine, Myocarde (anatomopathologie), Myocardite (anatomopathologie), Myocardite (étiologie), Mâle, Rayons X, Souris, Souris nude, Thymus (glande) (physiologie), Virus de la grippe A (croissance et développement).
- MESH :
- anatomopathologie : Myocarde, Myocardite.
- croissance et développement : Virus de la grippe A.
- microbiologie : Coeur.
- physiologie : Thymus (glande).
- étiologie : Myocardite.
- Animaux, Femelle, Infections à Orthomyxoviridae, Modèles animaux de maladie humaine, Mâle, Rayons X, Souris, Souris nude.
English descriptors
- KwdEn :
- MESH :
- complications : Orthomyxoviridae Infections.
- etiology : Myocarditis.
- growth & development : Influenza A virus.
- microbiology : Heart.
- pathology : Myocarditis, Myocardium.
- physiology : Thymus Gland.
- Animals, Disease Models, Animal, Female, Male, Mice, Mice, Nude, X-Rays.
Abstract
A mouse model was established for the study of acute myocarditis that occurs during influenza infection. Challenge with more than 10 LD50 of mouse‐adapted influenza A2 virus (H2N2) induced myocarditis macroscopically discernible as white, irregularly shaped lesions which were shown by histological examination to consist of necrotic myofibers surrounded by infiltrating mononuclear inflammatory cells. After challenge with 10 LD50 of the virus, macroscopic myocarditis was found to advance in a progressive manner up to the 7th day, while the virus titer in the heart reached its peak on the 2nd day and began to decrease on the 5th day of infection. However, development of myocarditis was significantly suppressed in mice which were irradiated with 400 R of X‐rays before infection. In addition, myocarditis did not develop in congenitally athymic nude mice. These data indicate that myocarditis was not brought about by viral action directly, but that it was mediated by some function of the host against viral in‐vasion, which was abolished by X‐irradiation. The data also suggest that T cells played a key role in the development of myocarditis.
Url:
DOI: 10.1111/j.1348-0421.1981.tb00020.x
Affiliations:
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Le document en format XML
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scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Male</term><term>Mice</term><term>Mice, Nude</term><term>X-Rays</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Infections à Orthomyxoviridae</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Rayons X</term><term>Souris</term><term>Souris nude</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">A mouse model was established for the study of acute myocarditis that occurs during influenza infection. Challenge with more than 10 LD50 of mouse‐adapted influenza A2 virus (H2N2) induced myocarditis macroscopically discernible as white, irregularly shaped lesions which were shown by histological examination to consist of necrotic myofibers surrounded by infiltrating mononuclear inflammatory cells. After challenge with 10 LD50 of the virus, macroscopic myocarditis was found to advance in a progressive manner up to the 7th day, while the virus titer in the heart reached its peak on the 2nd day and began to decrease on the 5th day of infection. However, development of myocarditis was significantly suppressed in mice which were irradiated with 400 R of X‐rays before infection. In addition, myocarditis did not develop in congenitally athymic nude mice. These data indicate that myocarditis was not brought about by viral action directly, but that it was mediated by some function of the host against viral in‐vasion, which was abolished by X‐irradiation. The data also suggest that T cells played a key role in the development of myocarditis.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Arai, Sumio" sort="Arai, Sumio" uniqKey="Arai S" first="Sumio" last="Arai">Sumio Arai</name><name sortKey="Ishida, Nakao" sort="Ishida, Nakao" uniqKey="Ishida N" first="Nakao" last="Ishida">Nakao Ishida</name><name sortKey="Sakamoto, Masahiro" sort="Sakamoto, Masahiro" uniqKey="Sakamoto M" first="Masahiro" last="Sakamoto">Masahiro Sakamoto</name><name sortKey="Suzuki, Fujio" sort="Suzuki, Fujio" uniqKey="Suzuki F" first="Fujio" last="Suzuki">Fujio Suzuki</name><name sortKey="Takishima, Tamotsu" sort="Takishima, Tamotsu" uniqKey="Takishima T" first="Tamotsu" last="Takishima">Tamotsu Takishima</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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