SrasV1, PubMed, Checkpoint, bibRecord, 001D44

Participation of both host and virus factors in induction of severe acute respiratory syndrome (SARS) in F344 rats infected with SARS coronavirus.

Identifieur interne : 001D44 ( PubMed/Checkpoint ); précédent : 001D43; suivant : 001D45

Participation of both host and virus factors in induction of severe acute respiratory syndrome (SARS) in F344 rats infected with SARS coronavirus.

Auteurs : Noriyo Nagata [Japon] ; Naoko Iwata ; Hideki Hasegawa ; Shuetsu Fukushi ; Masaru Yokoyama ; Ayako Harashima ; Yuko Sato ; Masayuki Saijo ; Shigeru Morikawa ; Tetsutaro Sata

Source :

Journal of virology [ 0022-538X ] ; 2007.

RBID : pubmed:17151094

Descripteurs français

KwdFr :
- Animaux, Cellules Vero, Cytokines (biosynthèse), Facteurs de l'âge, Femelle, Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (), Glycoprotéines membranaires (physiologie), Hémagglutinines virales (physiologie), Modèles animaux de maladie humaine, Modèles moléculaires, Passage en série, Peptidyl-Dipeptidase A (), Peptidyl-Dipeptidase A (métabolisme), Protéines de l'enveloppe virale (), Protéines de l'enveloppe virale (physiologie), Rats, Rats de lignée F344, Récepteurs viraux (métabolisme), Structure tertiaire des protéines (physiologie), Substitution d'acide aminé, Syndrome respiratoire aigu sévère (virologie), Virulence, Virus du SRAS (), Virus du SRAS (génétique), Virus du SRAS (pathogénicité).
MESH :
- biosynthèse : Cytokines.
- génétique : Virus du SRAS.
- métabolisme : Peptidyl-Dipeptidase A, Récepteurs viraux.
- pathogénicité : Virus du SRAS.
- physiologie : Glycoprotéines membranaires, Hémagglutinines virales, Protéines de l'enveloppe virale, Structure tertiaire des protéines.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Cellules Vero, Facteurs de l'âge, Femelle, Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires, Modèles animaux de maladie humaine, Modèles moléculaires, Passage en série, Peptidyl-Dipeptidase A, Protéines de l'enveloppe virale, Rats, Rats de lignée F344, Substitution d'acide aminé, Virulence, Virus du SRAS.

English descriptors

KwdEn :
- Age Factors, Amino Acid Substitution, Animals, Chlorocebus aethiops, Cytokines (biosynthesis), Disease Models, Animal, Female, Hemagglutinins, Viral (physiology), Membrane Glycoproteins (chemistry), Membrane Glycoproteins (physiology), Models, Molecular, Peptidyl-Dipeptidase A (chemistry), Peptidyl-Dipeptidase A (metabolism), Protein Structure, Tertiary (physiology), Rats, Rats, Inbred F344, Receptors, Virus (metabolism), SARS Virus (chemistry), SARS Virus (genetics), SARS Virus (pathogenicity), Serial Passage, Severe Acute Respiratory Syndrome (virology), Spike Glycoprotein, Coronavirus, Vero Cells, Viral Envelope Proteins (chemistry), Viral Envelope Proteins (physiology), Virulence.
MESH :
- chemical , biosynthesis : Cytokines.
- chemical , chemistry : Membrane Glycoproteins, Peptidyl-Dipeptidase A, Viral Envelope Proteins.
- chemical , metabolism : Peptidyl-Dipeptidase A, Receptors, Virus.
- chemical , physiology : Hemagglutinins, Viral, Membrane Glycoproteins, Viral Envelope Proteins.
- chemistry : SARS Virus.
- genetics : SARS Virus.
- pathogenicity : SARS Virus.
- physiology : Protein Structure, Tertiary.
- virology : Severe Acute Respiratory Syndrome.
- Age Factors, Amino Acid Substitution, Animals, Chlorocebus aethiops, Disease Models, Animal, Female, Models, Molecular, Rats, Rats, Inbred F344, Serial Passage, Spike Glycoprotein, Coronavirus, Vero Cells, Virulence.

Abstract

To understand the pathogenesis and develop an animal model of severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV), the Frankfurt 1 SARS-CoV isolate was passaged serially in young F344 rats. Young rats were susceptible to SARS-CoV but cleared the virus rapidly within 3 to 5 days of intranasal inoculation. After 10 serial passages, replication and virulence of SARS-CoV were increased in the respiratory tract of young rats without clinical signs. By contrast, adult rats infected with the passaged virus showed respiratory symptoms and severe pathological lesions in the lung. Levels of inflammatory cytokines in sera and lung tissues were significantly higher in adult F344 rats than in young rats. During in vivo passage of SARS-CoV, a single amino acid substitution was introduced within the binding domain of the viral spike protein recognizing angiotensin-converting enzyme 2 (ACE2), which is known as a SARS-CoV receptor. The rat-passaged virus more efficiently infected CHO cells expressing rat ACE2 than did the original isolate. These results strongly indicate that host and virus factors such as advanced age and virus adaptation are critical for the development of SARS in rats.

DOI: 10.1128/JVI.01967-06
PubMed: 17151094

Affiliations:

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to stream PubMed, to step Corpus: 001F64
to stream PubMed, to step Curation: 001F64

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Le document en format XML

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<term>Animals</term>
<term>Chlorocebus aethiops</term>
<term>Cytokines (biosynthesis)</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Hemagglutinins, Viral (physiology)</term>
<term>Membrane Glycoproteins (chemistry)</term>
<term>Membrane Glycoproteins (physiology)</term>
<term>Models, Molecular</term>
<term>Peptidyl-Dipeptidase A (chemistry)</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
<term>Protein Structure, Tertiary (physiology)</term>
<term>Rats</term>
<term>Rats, Inbred F344</term>
<term>Receptors, Virus (metabolism)</term>
<term>SARS Virus (chemistry)</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (pathogenicity)</term>
<term>Serial Passage</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Spike Glycoprotein, Coronavirus</term>
<term>Vero Cells</term>
<term>Viral Envelope Proteins (chemistry)</term>
<term>Viral Envelope Proteins (physiology)</term>
<term>Virulence</term>
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<term>Cytokines (biosynthèse)</term>
<term>Facteurs de l'âge</term>
<term>Femelle</term>
<term>Glycoprotéine de spicule des coronavirus</term>
<term>Glycoprotéines membranaires ()</term>
<term>Glycoprotéines membranaires (physiologie)</term>
<term>Hémagglutinines virales (physiologie)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Modèles moléculaires</term>
<term>Passage en série</term>
<term>Peptidyl-Dipeptidase A ()</term>
<term>Peptidyl-Dipeptidase A (métabolisme)</term>
<term>Protéines de l'enveloppe virale ()</term>
<term>Protéines de l'enveloppe virale (physiologie)</term>
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<term>Rats de lignée F344</term>
<term>Récepteurs viraux (métabolisme)</term>
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<term>Substitution d'acide aminé</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Virulence</term>
<term>Virus du SRAS ()</term>
<term>Virus du SRAS (génétique)</term>
<term>Virus du SRAS (pathogénicité)</term>
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<term>Peptidyl-Dipeptidase A</term>
<term>Viral Envelope Proteins</term>
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<term>Membrane Glycoproteins</term>
<term>Viral Envelope Proteins</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus du SRAS</term>
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<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Glycoprotéines membranaires</term>
<term>Hémagglutinines virales</term>
<term>Protéines de l'enveloppe virale</term>
<term>Structure tertiaire des protéines</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Protein Structure, Tertiary</term>
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<keywords scheme="MESH" xml:lang="en"><term>Age Factors</term>
<term>Amino Acid Substitution</term>
<term>Animals</term>
<term>Chlorocebus aethiops</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Models, Molecular</term>
<term>Rats</term>
<term>Rats, Inbred F344</term>
<term>Serial Passage</term>
<term>Spike Glycoprotein, Coronavirus</term>
<term>Vero Cells</term>
<term>Virulence</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules Vero</term>
<term>Facteurs de l'âge</term>
<term>Femelle</term>
<term>Glycoprotéine de spicule des coronavirus</term>
<term>Glycoprotéines membranaires</term>
<term>Modèles animaux de maladie humaine</term>
<term>Modèles moléculaires</term>
<term>Passage en série</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Protéines de l'enveloppe virale</term>
<term>Rats</term>
<term>Rats de lignée F344</term>
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<front><div type="abstract" xml:lang="en">To understand the pathogenesis and develop an animal model of severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV), the Frankfurt 1 SARS-CoV isolate was passaged serially in young F344 rats. Young rats were susceptible to SARS-CoV but cleared the virus rapidly within 3 to 5 days of intranasal inoculation. After 10 serial passages, replication and virulence of SARS-CoV were increased in the respiratory tract of young rats without clinical signs. By contrast, adult rats infected with the passaged virus showed respiratory symptoms and severe pathological lesions in the lung. Levels of inflammatory cytokines in sera and lung tissues were significantly higher in adult F344 rats than in young rats. During in vivo passage of SARS-CoV, a single amino acid substitution was introduced within the binding domain of the viral spike protein recognizing angiotensin-converting enzyme 2 (ACE2), which is known as a SARS-CoV receptor. The rat-passaged virus more efficiently infected CHO cells expressing rat ACE2 than did the original isolate. These results strongly indicate that host and virus factors such as advanced age and virus adaptation are critical for the development of SARS in rats.</div>
</front>
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<DateCompleted><Year>2007</Year>
<Month>03</Month>
<Day>20</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>04</Month>
<Day>15</Day>
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<Issue>4</Issue>
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<Title>Journal of virology</Title>
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<ArticleTitle>Participation of both host and virus factors in induction of severe acute respiratory syndrome (SARS) in F344 rats infected with SARS coronavirus.</ArticleTitle>
<Pagination><MedlinePgn>1848-57</MedlinePgn>
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<Abstract><AbstractText>To understand the pathogenesis and develop an animal model of severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV), the Frankfurt 1 SARS-CoV isolate was passaged serially in young F344 rats. Young rats were susceptible to SARS-CoV but cleared the virus rapidly within 3 to 5 days of intranasal inoculation. After 10 serial passages, replication and virulence of SARS-CoV were increased in the respiratory tract of young rats without clinical signs. By contrast, adult rats infected with the passaged virus showed respiratory symptoms and severe pathological lesions in the lung. Levels of inflammatory cytokines in sera and lung tissues were significantly higher in adult F344 rats than in young rats. During in vivo passage of SARS-CoV, a single amino acid substitution was introduced within the binding domain of the viral spike protein recognizing angiotensin-converting enzyme 2 (ACE2), which is known as a SARS-CoV receptor. The rat-passaged virus more efficiently infected CHO cells expressing rat ACE2 than did the original isolate. These results strongly indicate that host and virus factors such as advanced age and virus adaptation are critical for the development of SARS in rats.</AbstractText>
</Abstract>
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<Initials>N</Initials>
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<Initials>S</Initials>
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<ArticleDate DateType="Electronic"><Year>2006</Year>
<Month>12</Month>
<Day>06</Day>
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Participation of both host and virus factors in induction of severe acute respiratory syndrome (SARS) in F344 rats infected with SARS coronavirus.

Participation of both host and virus factors in induction of severe acute respiratory syndrome (SARS) in F344 rats infected with SARS coronavirus.

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