Detection of severe acute respiratory syndrome coronavirus in the brain : Potential role of the chemokine mig in pathogenesis
Identifieur interne : 000573 ( PascalFrancis/Corpus ); précédent : 000572; suivant : 000574Detection of severe acute respiratory syndrome coronavirus in the brain : Potential role of the chemokine mig in pathogenesis
Auteurs : JUN XU ; SHUQING ZHONG ; JINGHUA LIU ; LI LI ; YONG LI ; XINWEI WU ; ZHIJIE LI ; PENG DENG ; JINGQIANG ZHANG ; NANSHAN ZHONG ; YANQING DING ; YONG JIANGSource :
- Clinical infectious diseases [ 1058-4838 ] ; 2005.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Background. Previous studies have shown that common human coronavirus might be neurotropic, although it was first isolated as a pathogen of the respiratory tract. We noticed that a few patients with severe acute respiratory syndrome (SARS) experienced central nervous symptoms during the course of illness. In the present study, we isolated a SARS coronavirus strain from a brain tissue specimen obtained from a patient with SARS with significant central nervous symptoms. Methods. Using transmission electronic microscopy and nested reverse transcription-polymerase chain reaction, the causative pathogen was identified in cultures of a brain tissue specimen obtained from the patient with SARS. Histopathologic examination of the brain tissue was performed using the methods of immunohistochemistry analysis and double immunofluorescence staining. Fifteen cytokines and chemokines were detected in the blood of the patient with SARS by means of a bead-based multiassay system. Results. A fragment specific for SARS human coronavirus was amplified from cultures of the brain suspension, and transmission electronic microscopy revealed the presence of an enveloped virus morphologically compatible with a coronavirus isolated in the cultures. Pathologic examination of the brain tissue revealed necrosis of neuron cells and broad hyperplasia of gliocytes. Immunostaining demonstrated that monokine induced by interferon-γ (Mig) was expressed in gliocytes with the infiltration of CD68+ monocytes/macrophages and CD3+ T lymphocytes in the brain mesenchyme. Cytokine/chemokine assay revealed that levels of interferon-γ-inducible protein 10 and Mig in the blood were highly elevated, although the levels of other cytokines and chemokines were close to normal. Conclusions. This study provides direct evidence that SARS human coronavirus is capable of infecting the central nervous system, and that Mig might be involved in the brain immunopathology of SARS.
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Format Inist (serveur)
NO : | PASCAL 06-0000179 INIST |
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ET : | Detection of severe acute respiratory syndrome coronavirus in the brain : Potential role of the chemokine mig in pathogenesis |
AU : | JUN XU; SHUQING ZHONG; JINGHUA LIU; LI LI; YONG LI; XINWEI WU; ZHIJIE LI; PENG DENG; JINGQIANG ZHANG; NANSHAN ZHONG; YANQING DING; YONG JIANG |
AF : | Guangzhou Institute of Respiratory Diseases, Southern Medical University/Chine (1 aut., 2 aut., 4 aut., 5 aut., 10 aut.); Key Laboratory of Functional Proteomics of Guangdong Province, Southern Medical University/Chine (3 aut., 7 aut., 8 aut., 11 aut., 12 aut.); Guangzhou Center for Diseases Control and Prevention, Sun Yatsen University/Guangzhou/Chine (6 aut.); Electronic Microscope Center, Sun Yatsen University/Guangzhou/Chine (9 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Clinical infectious diseases; ISSN 1058-4838; Coden CIDIEL; Etats-Unis; Da. 2005; Vol. 41; No. 8; Pp. 1089-1096; Bibl. 30 ref. |
LA : | Anglais |
EA : | Background. Previous studies have shown that common human coronavirus might be neurotropic, although it was first isolated as a pathogen of the respiratory tract. We noticed that a few patients with severe acute respiratory syndrome (SARS) experienced central nervous symptoms during the course of illness. In the present study, we isolated a SARS coronavirus strain from a brain tissue specimen obtained from a patient with SARS with significant central nervous symptoms. Methods. Using transmission electronic microscopy and nested reverse transcription-polymerase chain reaction, the causative pathogen was identified in cultures of a brain tissue specimen obtained from the patient with SARS. Histopathologic examination of the brain tissue was performed using the methods of immunohistochemistry analysis and double immunofluorescence staining. Fifteen cytokines and chemokines were detected in the blood of the patient with SARS by means of a bead-based multiassay system. Results. A fragment specific for SARS human coronavirus was amplified from cultures of the brain suspension, and transmission electronic microscopy revealed the presence of an enveloped virus morphologically compatible with a coronavirus isolated in the cultures. Pathologic examination of the brain tissue revealed necrosis of neuron cells and broad hyperplasia of gliocytes. Immunostaining demonstrated that monokine induced by interferon-γ (Mig) was expressed in gliocytes with the infiltration of CD68+ monocytes/macrophages and CD3+ T lymphocytes in the brain mesenchyme. Cytokine/chemokine assay revealed that levels of interferon-γ-inducible protein 10 and Mig in the blood were highly elevated, although the levels of other cytokines and chemokines were close to normal. Conclusions. This study provides direct evidence that SARS human coronavirus is capable of infecting the central nervous system, and that Mig might be involved in the brain immunopathology of SARS. |
CC : | 002B05C02C |
FD : | Syndrome respiratoire aigu sévère; Encéphale; Cerveau; Chimiokine; Coronavirus; Pathogénie |
FG : | Virose; Infection; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie |
ED : | Severe acute respiratory syndrome; Encephalon; Brain; Chemokine; Coronavirus; Pathogenesis |
EG : | Viral disease; Infection; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease |
SD : | Síndrome respiratorio agudo severo; Encéfalo; Cerebro; Quimioquina; Coronavirus; Patogenia |
LO : | INIST-18407.354000131931080020 |
ID : | 06-0000179 |
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<series><title level="j" type="main">Clinical infectious diseases</title>
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<term>Pathogenesis</term>
<term>Severe acute respiratory syndrome</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
<term>Encéphale</term>
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<front><div type="abstract" xml:lang="en">Background. Previous studies have shown that common human coronavirus might be neurotropic, although it was first isolated as a pathogen of the respiratory tract. We noticed that a few patients with severe acute respiratory syndrome (SARS) experienced central nervous symptoms during the course of illness. In the present study, we isolated a SARS coronavirus strain from a brain tissue specimen obtained from a patient with SARS with significant central nervous symptoms. Methods. Using transmission electronic microscopy and nested reverse transcription-polymerase chain reaction, the causative pathogen was identified in cultures of a brain tissue specimen obtained from the patient with SARS. Histopathologic examination of the brain tissue was performed using the methods of immunohistochemistry analysis and double immunofluorescence staining. Fifteen cytokines and chemokines were detected in the blood of the patient with SARS by means of a bead-based multiassay system. Results. A fragment specific for SARS human coronavirus was amplified from cultures of the brain suspension, and transmission electronic microscopy revealed the presence of an enveloped virus morphologically compatible with a coronavirus isolated in the cultures. Pathologic examination of the brain tissue revealed necrosis of neuron cells and broad hyperplasia of gliocytes. Immunostaining demonstrated that monokine induced by interferon-γ (Mig) was expressed in gliocytes with the infiltration of CD68<sup>+</sup>
monocytes/macrophages and CD3<sup>+</sup>
T lymphocytes in the brain mesenchyme. Cytokine/chemokine assay revealed that levels of interferon-γ-inducible protein 10 and Mig in the blood were highly elevated, although the levels of other cytokines and chemokines were close to normal. Conclusions. This study provides direct evidence that SARS human coronavirus is capable of infecting the central nervous system, and that Mig might be involved in the brain immunopathology of SARS.</div>
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<fC01 i1="01" l="ENG"><s0>Background. Previous studies have shown that common human coronavirus might be neurotropic, although it was first isolated as a pathogen of the respiratory tract. We noticed that a few patients with severe acute respiratory syndrome (SARS) experienced central nervous symptoms during the course of illness. In the present study, we isolated a SARS coronavirus strain from a brain tissue specimen obtained from a patient with SARS with significant central nervous symptoms. Methods. Using transmission electronic microscopy and nested reverse transcription-polymerase chain reaction, the causative pathogen was identified in cultures of a brain tissue specimen obtained from the patient with SARS. Histopathologic examination of the brain tissue was performed using the methods of immunohistochemistry analysis and double immunofluorescence staining. Fifteen cytokines and chemokines were detected in the blood of the patient with SARS by means of a bead-based multiassay system. Results. A fragment specific for SARS human coronavirus was amplified from cultures of the brain suspension, and transmission electronic microscopy revealed the presence of an enveloped virus morphologically compatible with a coronavirus isolated in the cultures. Pathologic examination of the brain tissue revealed necrosis of neuron cells and broad hyperplasia of gliocytes. Immunostaining demonstrated that monokine induced by interferon-γ (Mig) was expressed in gliocytes with the infiltration of CD68<sup>+</sup>
monocytes/macrophages and CD3<sup>+</sup>
T lymphocytes in the brain mesenchyme. Cytokine/chemokine assay revealed that levels of interferon-γ-inducible protein 10 and Mig in the blood were highly elevated, although the levels of other cytokines and chemokines were close to normal. Conclusions. This study provides direct evidence that SARS human coronavirus is capable of infecting the central nervous system, and that Mig might be involved in the brain immunopathology of SARS.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B05C02C</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>07</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>07</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Cerveau</s0>
<s5>08</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Brain</s0>
<s5>08</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Cerebro</s0>
<s5>08</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Chimiokine</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Chemokine</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Quimioquina</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Pathogénie</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Pathogenesis</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Patogenia</s0>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>38</s5>
</fC07>
<fN21><s1>002</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
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<server><NO>PASCAL 06-0000179 INIST</NO>
<ET>Detection of severe acute respiratory syndrome coronavirus in the brain : Potential role of the chemokine mig in pathogenesis</ET>
<AU>JUN XU; SHUQING ZHONG; JINGHUA LIU; LI LI; YONG LI; XINWEI WU; ZHIJIE LI; PENG DENG; JINGQIANG ZHANG; NANSHAN ZHONG; YANQING DING; YONG JIANG</AU>
<AF>Guangzhou Institute of Respiratory Diseases, Southern Medical University/Chine (1 aut., 2 aut., 4 aut., 5 aut., 10 aut.); Key Laboratory of Functional Proteomics of Guangdong Province, Southern Medical University/Chine (3 aut., 7 aut., 8 aut., 11 aut., 12 aut.); Guangzhou Center for Diseases Control and Prevention, Sun Yatsen University/Guangzhou/Chine (6 aut.); Electronic Microscope Center, Sun Yatsen University/Guangzhou/Chine (9 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Clinical infectious diseases; ISSN 1058-4838; Coden CIDIEL; Etats-Unis; Da. 2005; Vol. 41; No. 8; Pp. 1089-1096; Bibl. 30 ref.</SO>
<LA>Anglais</LA>
<EA>Background. Previous studies have shown that common human coronavirus might be neurotropic, although it was first isolated as a pathogen of the respiratory tract. We noticed that a few patients with severe acute respiratory syndrome (SARS) experienced central nervous symptoms during the course of illness. In the present study, we isolated a SARS coronavirus strain from a brain tissue specimen obtained from a patient with SARS with significant central nervous symptoms. Methods. Using transmission electronic microscopy and nested reverse transcription-polymerase chain reaction, the causative pathogen was identified in cultures of a brain tissue specimen obtained from the patient with SARS. Histopathologic examination of the brain tissue was performed using the methods of immunohistochemistry analysis and double immunofluorescence staining. Fifteen cytokines and chemokines were detected in the blood of the patient with SARS by means of a bead-based multiassay system. Results. A fragment specific for SARS human coronavirus was amplified from cultures of the brain suspension, and transmission electronic microscopy revealed the presence of an enveloped virus morphologically compatible with a coronavirus isolated in the cultures. Pathologic examination of the brain tissue revealed necrosis of neuron cells and broad hyperplasia of gliocytes. Immunostaining demonstrated that monokine induced by interferon-γ (Mig) was expressed in gliocytes with the infiltration of CD68<sup>+</sup>
monocytes/macrophages and CD3<sup>+</sup>
T lymphocytes in the brain mesenchyme. Cytokine/chemokine assay revealed that levels of interferon-γ-inducible protein 10 and Mig in the blood were highly elevated, although the levels of other cytokines and chemokines were close to normal. Conclusions. This study provides direct evidence that SARS human coronavirus is capable of infecting the central nervous system, and that Mig might be involved in the brain immunopathology of SARS.</EA>
<CC>002B05C02C</CC>
<FD>Syndrome respiratoire aigu sévère; Encéphale; Cerveau; Chimiokine; Coronavirus; Pathogénie</FD>
<FG>Virose; Infection; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie</FG>
<ED>Severe acute respiratory syndrome; Encephalon; Brain; Chemokine; Coronavirus; Pathogenesis</ED>
<EG>Viral disease; Infection; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease</EG>
<SD>Síndrome respiratorio agudo severo; Encéfalo; Cerebro; Quimioquina; Coronavirus; Patogenia</SD>
<LO>INIST-18407.354000131931080020</LO>
<ID>06-0000179</ID>
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