Serveur d'exploration SRAS

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Molecular mechanisms of severe acute respiratory syndrome (SARS)

Identifieur interne : 000460 ( Pmc/Curation ); précédent : 000459; suivant : 000461

Molecular mechanisms of severe acute respiratory syndrome (SARS)

Auteurs : David A. Groneberg [Allemagne] ; Rolf Hilgenfeld [Allemagne] ; Peter Zabel [Allemagne]

Source :

RBID : PMC:548145

Abstract

Severe acute respiratory syndrome (SARS) is a new infectious disease caused by a novel coronavirus that leads to deleterious pulmonary pathological features. Due to its high morbidity and mortality and widespread occurrence, SARS has evolved as an important respiratory disease which may be encountered everywhere in the world. The virus was identified as the causative agent of SARS due to the efforts of a WHO-led laboratory network. The potential mutability of the SARS-CoV genome may lead to new SARS outbreaks and several regions of the viral genomes open reading frames have been identified which may contribute to the severe virulence of the virus. With regard to the pathogenesis of SARS, several mechanisms involving both direct effects on target cells and indirect effects via the immune system may exist. Vaccination would offer the most attractive approach to prevent new epidemics of SARS, but the development of vaccines is difficult due to missing data on the role of immune system-virus interactions and the potential mutability of the virus. Even in a situation of no new infections, SARS remains a major health hazard, as new epidemics may arise. Therefore, further experimental and clinical research is required to control the disease.


Url:
DOI: 10.1186/1465-9921-6-8
PubMed: 15661082
PubMed Central: 548145

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PMC:548145

Le document en format XML

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<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Respir Res</journal-id>
<journal-id journal-id-type="iso-abbrev">Respir. Res</journal-id>
<journal-title-group>
<journal-title>Respiratory Research</journal-title>
</journal-title-group>
<issn pub-type="ppub">1465-9921</issn>
<issn pub-type="epub">1465-993X</issn>
<publisher>
<publisher-name>BioMed Central</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">15661082</article-id>
<article-id pub-id-type="pmc">548145</article-id>
<article-id pub-id-type="publisher-id">246</article-id>
<article-id pub-id-type="doi">10.1186/1465-9921-6-8</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Review</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Molecular mechanisms of severe acute respiratory syndrome (SARS)</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Groneberg</surname>
<given-names>David A</given-names>
</name>
<address>
<email>david.groneberg@charite.de</email>
</address>
<xref ref-type="aff" rid="Aff1_246">1_246</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Hilgenfeld</surname>
<given-names>Rolf</given-names>
</name>
<address>
<email>hilgenfeld@biochem.uni-luebeck.de</email>
</address>
<xref ref-type="aff" rid="Aff2_246">2_246</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zabel</surname>
<given-names>Peter</given-names>
</name>
<address>
<email>pzabel@fz-borstel.de</email>
</address>
<xref ref-type="aff" rid="Aff3_246">3_246</xref>
<xref ref-type="aff" rid="Aff4_246">4_246</xref>
</contrib>
<aff id="Aff1_246">
<label>1_246</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.7468.d</institution-id>
<institution-id institution-id-type="ISNI">0000000122487639</institution-id>
<institution>Pneumology and Immunology, Otto-Heubner-Centre,</institution>
<institution>Charité School of Medicine, Free University and Humboldt-University,</institution>
</institution-wrap>
D-13353 Berlin, Germany</aff>
<aff id="Aff2_246">
<label>2_246</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.4562.5</institution-id>
<institution-id institution-id-type="ISNI">0000000100572672</institution-id>
<institution>Institute of Biochemistry,</institution>
<institution>University of Lübeck,</institution>
</institution-wrap>
D-23538 Lübeck, Germany</aff>
<aff id="Aff3_246">
<label>3_246</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.418187.3</institution-id>
<institution-id institution-id-type="ISNI">0000000404939170</institution-id>
<institution>Division of Clinical Infectiology and Immunology, Department of Medicine,</institution>
<institution>Research Center Borstel,</institution>
</institution-wrap>
D-23845 Borstel, Germany</aff>
<aff id="Aff4_246">
<label>4_246</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.4562.5</institution-id>
<institution-id institution-id-type="ISNI">0000000100572672</institution-id>
<institution>Division of Thoracic Medicine, Department of Medicine,</institution>
<institution>University of Lübeck,</institution>
</institution-wrap>
D-23538 Lübeck, Germany</aff>
</contrib-group>
<pub-date pub-type="epub">
<day>20</day>
<month>1</month>
<year>2005</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>20</day>
<month>1</month>
<year>2005</year>
</pub-date>
<pub-date pub-type="ppub">
<year>2005</year>
</pub-date>
<volume>6</volume>
<elocation-id>8</elocation-id>
<history>
<date date-type="received">
<day>10</day>
<month>11</month>
<year>2004</year>
</date>
<date date-type="accepted">
<day>20</day>
<month>1</month>
<year>2005</year>
</date>
</history>
<permissions>
<copyright-statement>© Groneberg et al. 2005</copyright-statement>
<license>
<license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p>
</license>
</permissions>
<abstract id="Abs1_246">
<p>Severe acute respiratory syndrome (SARS) is a new infectious disease caused by a novel coronavirus that leads to deleterious pulmonary pathological features. Due to its high morbidity and mortality and widespread occurrence, SARS has evolved as an important respiratory disease which may be encountered everywhere in the world. The virus was identified as the causative agent of SARS due to the efforts of a WHO-led laboratory network. The potential mutability of the SARS-CoV genome may lead to new SARS outbreaks and several regions of the viral genomes open reading frames have been identified which may contribute to the severe virulence of the virus. With regard to the pathogenesis of SARS, several mechanisms involving both direct effects on target cells and indirect effects via the immune system may exist. Vaccination would offer the most attractive approach to prevent new epidemics of SARS, but the development of vaccines is difficult due to missing data on the role of immune system-virus interactions and the potential mutability of the virus. Even in a situation of no new infections, SARS remains a major health hazard, as new epidemics may arise. Therefore, further experimental and clinical research is required to control the disease.</p>
</abstract>
<kwd-group xml:lang="en">
<kwd>Severe Acute Respiratory Syndrome</kwd>
<kwd>SARS</kwd>
<kwd>coronavirus</kwd>
<kwd>molecular mechanisms</kwd>
<kwd>therapy</kwd>
<kwd>vaccination</kwd>
</kwd-group>
<custom-meta-group>
<custom-meta>
<meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2005</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>

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