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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

Identifieur interne : 000585 ( PascalFrancis/Curation ); précédent : 000584; suivant : 000586

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 [Japon] ; Hideki Hasegawa [Japon] ; Shuetsu Fukushi [Japon] ; Masaru Yokoyama [Japon] ; Ayako Harashima [Japon] ; Yuko Sato [Japon] ; Masayuki Saijo [Japon] ; Shigeru Morikawa [Japon] ; Tetsutaro Sata [Japon]

Source :

RBID : Pascal:07-0121593

Descripteurs français

English descriptors

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.
pA  
A01 01  1    @0 0022-538X
A03   1    @0 J. virol.
A05       @2 81
A06       @2 4
A08 01  1  ENG  @1 Participation of both host and virus factors in induction of severe acute respiratory syndrome (SARS) in F344 Rats infected with SARS coronavirus
A11 01  1    @1 NAGATA (Noriyo)
A11 02  1    @1 IWATA (Naoko)
A11 03  1    @1 HASEGAWA (Hideki)
A11 04  1    @1 FUKUSHI (Shuetsu)
A11 05  1    @1 YOKOYAMA (Masaru)
A11 06  1    @1 HARASHIMA (Ayako)
A11 07  1    @1 SATO (Yuko)
A11 08  1    @1 SAIJO (Masayuki)
A11 09  1    @1 MORIKAWA (Shigeru)
A11 10  1    @1 SATA (Tetsutaro)
A14 01      @1 Department of Pathology, National Institute of Infectious Diseases @2 Tokyo @3 JPN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 6 aut. @Z 7 aut. @Z 10 aut.
A14 02      @1 Department of Virology I, National Institute of Infectious Diseases @2 Tokyo @3 JPN @Z 4 aut. @Z 8 aut. @Z 9 aut.
A14 03      @1 Center for Pathogen Genomics, National Institute of Infectious Diseases @2 Tokyo @3 JPN @Z 5 aut.
A20       @1 1848-1857
A21       @1 2007
A23 01      @0 ENG
A43 01      @1 INIST @2 13592 @5 354000159785480290
A44       @0 0000 @1 © 2007 INIST-CNRS. All rights reserved.
A45       @0 40 ref.
A47 01  1    @0 07-0121593
A60       @1 P
A61       @0 A
A64 01  1    @0 Journal of virology
A66 01      @0 USA
C01 01    ENG  @0 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.
C02 01  X    @0 002A05C10
C03 01  X  FRE  @0 Virus syndrome respiratoire aigu sévère @2 NW @5 01
C03 01  X  ENG  @0 Severe acute respiratory syndrome virus @2 NW @5 01
C03 01  X  SPA  @0 Severe acute respiratory syndrome virus @2 NW @5 01
C03 02  X  FRE  @0 Coronavirus rat @2 NW @5 02
C03 02  X  ENG  @0 Rat coronavirus @2 NW @5 02
C03 02  X  SPA  @0 Rat coronavirus @2 NW @5 02
C03 03  X  FRE  @0 Virologie @5 05
C03 03  X  ENG  @0 Virology @5 05
C03 03  X  SPA  @0 Virología @5 05
C03 04  X  FRE  @0 Syndrome respiratoire aigu sévère @2 NM @5 14
C03 04  X  ENG  @0 Severe acute respiratory syndrome @2 NM @5 14
C03 04  X  SPA  @0 Síndrome respiratorio agudo severo @2 NM @5 14
C07 01  X  FRE  @0 Coronavirus @2 NW
C07 01  X  ENG  @0 Coronavirus @2 NW
C07 01  X  SPA  @0 Coronavirus @2 NW
C07 02  X  FRE  @0 Coronaviridae @2 NW
C07 02  X  ENG  @0 Coronaviridae @2 NW
C07 02  X  SPA  @0 Coronaviridae @2 NW
C07 03  X  FRE  @0 Nidovirales @2 NW
C07 03  X  ENG  @0 Nidovirales @2 NW
C07 03  X  SPA  @0 Nidovirales @2 NW
C07 04  X  FRE  @0 Virus @2 NW
C07 04  X  ENG  @0 Virus @2 NW
C07 04  X  SPA  @0 Virus @2 NW
C07 05  X  FRE  @0 Appareil respiratoire pathologie @5 13
C07 05  X  ENG  @0 Respiratory disease @5 13
C07 05  X  SPA  @0 Aparato respiratorio patología @5 13
C07 06  X  FRE  @0 Virose
C07 06  X  ENG  @0 Viral disease
C07 06  X  SPA  @0 Virosis
C07 07  X  FRE  @0 Infection
C07 07  X  ENG  @0 Infection
C07 07  X  SPA  @0 Infección
C07 08  X  FRE  @0 Poumon pathologie @5 16
C07 08  X  ENG  @0 Lung disease @5 16
C07 08  X  SPA  @0 Pulmón patología @5 16
N21       @1 078
N44 01      @1 OTO
N82       @1 OTO

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Pascal:07-0121593

Le document en format XML

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<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>
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<s1>Department of Pathology, National Institute of Infectious Diseases</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Department of Virology I, National Institute of Infectious Diseases</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>4 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="03">
<s1>Center for Pathogen Genomics, National Institute of Infectious Diseases</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA20>
<s1>1848-1857</s1>
</fA20>
<fA21>
<s1>2007</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>13592</s2>
<s5>354000159785480290</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2007 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>40 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>07-0121593</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Journal of virology</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002A05C10</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Virus syndrome respiratoire aigu sévère</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Severe acute respiratory syndrome virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Severe acute respiratory syndrome virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Coronavirus rat</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Rat coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Rat coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Virologie</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Virology</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Virología</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Virose</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Viral disease</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Virosis</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Infection</s0>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Infection</s0>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Infección</s0>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21>
<s1>078</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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{{Explor lien
   |wiki=    Sante
   |area=    SrasV1
   |flux=    PascalFrancis
   |étape=   Curation
   |type=    RBID
   |clé=     Pascal:07-0121593
   |texte=   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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