Pathogenetic mechanisms of severe acute respiratory syndrome
Identifieur interne : 000F24 ( Pmc/Checkpoint ); précédent : 000F23; suivant : 000F25Pathogenetic mechanisms of severe acute respiratory syndrome
Auteurs : Yong Guo ; Christine Korteweg ; Michael A. Mcnutt ; Jiang GuSource :
- Virus Research [ 0168-1702 ] ; 2007.
Abstract
Severe acute respiratory syndrome (SARS) is an acute respiratory disease with significant morbidity and mortality. While its clinical manifestations have been extensively studied, its pathogenesis is not yet fully understood. A limited number of autopsy studies have revealed that the lungs and the immune system are the organs that sustain the most severe damage. Other organs affected include the kidneys, brain, digestive tract, heart, liver, thyroid gland and urogenital tract. The primary target cells are pneumocytes and enterocytes, both cell types abundantly expressing angiotensin-converting enzyme 2 which is the main SARS-CoV receptor. Other cell types infected include the epithelial cells of renal tubules, cerebral neurons, and immune cells. The pathology of this disease results from both direct and indirect injury. Direct injury is caused by infection of the target cells by the virus. Indirect injury mainly results from immune responses, circulatory dysfunction, and hypoxia. In this review, we summarize the major pathological findings at the gross, cellular and molecular levels and discuss the various possible mechanisms that may contribute to the pathogenesis of SARS. The implications of the proposed pathogenesis for prevention, diagnosis and therapy of the disease are discussed.
Url:
DOI: 10.1016/j.virusres.2007.01.022
PubMed: 17825937
PubMed Central: 7114157
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<front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome (SARS) is an acute respiratory disease with significant morbidity and mortality. While its clinical manifestations have been extensively studied, its pathogenesis is not yet fully understood. A limited number of autopsy studies have revealed that the lungs and the immune system are the organs that sustain the most severe damage. Other organs affected include the kidneys, brain, digestive tract, heart, liver, thyroid gland and urogenital tract. The primary target cells are pneumocytes and enterocytes, both cell types abundantly expressing angiotensin-converting enzyme 2 which is the main SARS-CoV receptor. Other cell types infected include the epithelial cells of renal tubules, cerebral neurons, and immune cells. The pathology of this disease results from both direct and indirect injury. Direct injury is caused by infection of the target cells by the virus. Indirect injury mainly results from immune responses, circulatory dysfunction, and hypoxia. In this review, we summarize the major pathological findings at the gross, cellular and molecular levels and discuss the various possible mechanisms that may contribute to the pathogenesis of SARS. The implications of the proposed pathogenesis for prevention, diagnosis and therapy of the disease are discussed.</p>
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</back>
</TEI>
<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Virus Res</journal-id>
<journal-id journal-id-type="iso-abbrev">Virus Res</journal-id>
<journal-title-group><journal-title>Virus Research</journal-title>
</journal-title-group>
<issn pub-type="ppub">0168-1702</issn>
<issn pub-type="epub">1872-7492</issn>
<publisher><publisher-name>Published by Elsevier B.V.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">17825937</article-id>
<article-id pub-id-type="pmc">7114157</article-id>
<article-id pub-id-type="publisher-id">S0168-1702(07)00266-3</article-id>
<article-id pub-id-type="doi">10.1016/j.virusres.2007.01.022</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Pathogenetic mechanisms of severe acute respiratory syndrome</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Guo</surname>
<given-names>Yong</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Korteweg</surname>
<given-names>Christine</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>McNutt</surname>
<given-names>Michael A.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Gu</surname>
<given-names>Jiang</given-names>
</name>
<email>jianggu@bjmu.edu.cn</email>
<xref rid="cor1" ref-type="corresp">⁎</xref>
</contrib>
</contrib-group>
<aff>Department of Pathology, School of Basic Medical Sciences, Peking (Beijing) University, 38 Xueyuan Road, 100083 Beijing, China</aff>
<author-notes><corresp id="cor1"><label>⁎</label>
Corresponding author at: Department of Pathology, School of Medical Sciences, Infectious Disease Center, Peking (Beijing) University, 38 Xueyuan Road, 100083 Beijing, China. Tel.: +86 10 8280 1237; fax: +86 10 8280 1380. <email>jianggu@bjmu.edu.cn</email>
</corresp>
</author-notes>
<pub-date pub-type="pmc-release"><day>7</day>
<month>9</month>
<year>2007</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>4</month>
<year>2008</year>
</pub-date>
<pub-date pub-type="epub"><day>7</day>
<month>9</month>
<year>2007</year>
</pub-date>
<volume>133</volume>
<issue>1</issue>
<fpage>4</fpage>
<lpage>12</lpage>
<permissions><copyright-statement>Copyright © 2007 Published by Elsevier B.V.</copyright-statement>
<copyright-year>2007</copyright-year>
<copyright-holder></copyright-holder>
<license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p>
</license>
</permissions>
<abstract><p>Severe acute respiratory syndrome (SARS) is an acute respiratory disease with significant morbidity and mortality. While its clinical manifestations have been extensively studied, its pathogenesis is not yet fully understood. A limited number of autopsy studies have revealed that the lungs and the immune system are the organs that sustain the most severe damage. Other organs affected include the kidneys, brain, digestive tract, heart, liver, thyroid gland and urogenital tract. The primary target cells are pneumocytes and enterocytes, both cell types abundantly expressing angiotensin-converting enzyme 2 which is the main SARS-CoV receptor. Other cell types infected include the epithelial cells of renal tubules, cerebral neurons, and immune cells. The pathology of this disease results from both direct and indirect injury. Direct injury is caused by infection of the target cells by the virus. Indirect injury mainly results from immune responses, circulatory dysfunction, and hypoxia. In this review, we summarize the major pathological findings at the gross, cellular and molecular levels and discuss the various possible mechanisms that may contribute to the pathogenesis of SARS. The implications of the proposed pathogenesis for prevention, diagnosis and therapy of the disease are discussed.</p>
</abstract>
<kwd-group><title>Keywords</title>
<kwd>SARS</kwd>
<kwd>Pathology</kwd>
<kwd>Immune system</kwd>
<kwd>Virus</kwd>
<kwd>Lung</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Gu, Jiang" sort="Gu, Jiang" uniqKey="Gu J" first="Jiang" last="Gu">Jiang Gu</name>
<name sortKey="Guo, Yong" sort="Guo, Yong" uniqKey="Guo Y" first="Yong" last="Guo">Yong Guo</name>
<name sortKey="Korteweg, Christine" sort="Korteweg, Christine" uniqKey="Korteweg C" first="Christine" last="Korteweg">Christine Korteweg</name>
<name sortKey="Mcnutt, Michael A" sort="Mcnutt, Michael A" uniqKey="Mcnutt M" first="Michael A." last="Mcnutt">Michael A. Mcnutt</name>
</noCountry>
</tree>
</affiliations>
</record>
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