SrasV1, PascalFrancis, Checkpoint, bibRecord, 000493

Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

Identifieur interne : 000493 ( PascalFrancis/Checkpoint ); précédent : 000492; suivant : 000494

Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

Auteurs : Tamaki Okabayashi [Japon] ; Hiroaki Kariwa [Japon] ; Shin-Ichi Yokota [Japon] ; Shigeo Iki [Japon] ; Tomokazu Indoh [Japon] ; Noriko Yokosawa [Japon] ; Ikuo Takashima [Japon] ; Hiroyuki Tsutsumi [Japon] ; Nobuhiro Fujii [Japon]

Source :

Journal of medical virology [ 0146-6615 ] ; 2006.

RBID : Pascal:06-0257225

Descripteurs français

Pascal (Inist)
- Virus syndrome respiratoire aigu sévère, Cytokine, Interleukine 6, Virose, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Cytokine, Interleukin 6, Severe acute respiratory syndrome, Severe acute respiratory syndrome virus, Viral disease.

Abstract

The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS. J. Med. Virol.

Affiliations:

Japon

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Le document en format XML

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<front><div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS. J. Med. Virol.</div>
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<fC03 i1="04" i2="X" l="SPA"><s0>Virosis</s0>
<s5>14</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>15</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>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>163</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations><list><country><li>Japon</li>
</country>
</list>
<tree><country name="Japon"><noRegion><name sortKey="Okabayashi, Tamaki" sort="Okabayashi, Tamaki" uniqKey="Okabayashi T" first="Tamaki" last="Okabayashi">Tamaki Okabayashi</name>
</noRegion>
<name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name>
<name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name>
<name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name>
<name sortKey="Kariwa, Hiroaki" sort="Kariwa, Hiroaki" uniqKey="Kariwa H" first="Hiroaki" last="Kariwa">Hiroaki Kariwa</name>
<name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name>
<name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name>
<name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name>
<name sortKey="Yokota, Shin Ichi" sort="Yokota, Shin Ichi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name>
</country>
</tree>
</affiliations>
</record>

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   |texte=   Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
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Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

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