Serveur d'exploration SRAS

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[Lung pathology and pathogenesis of severe acute respiratory syndrome: a report of six full autopsies].

Identifieur interne : 002361 ( PubMed/Checkpoint ); précédent : 002360; suivant : 002362

[Lung pathology and pathogenesis of severe acute respiratory syndrome: a report of six full autopsies].

Auteurs : Fei Pei [République populaire de Chine] ; Jie Zheng ; Zi-Fen Gao ; Yan-Feng Zhong ; Wei-Gang Fang ; En-Cong Gong ; Wan-Zhong Zou ; Sheng-Lan Wang ; Dong-Xia Gao ; Zhi-Gang Xie ; Min Lu ; Xue-Ying Shi ; Cong-Rong Liu ; Jing-Ping Yang ; Yu-Ping Wang ; Zhi-Hui Han ; Xiao-Hong Shi ; Wen-Bin Dao ; Jiang Gu

Source :

RBID : pubmed:16536279

Descripteurs français

English descriptors

Abstract

Severe acute respiratory syndrome (SARS) is an emerging infectious disease that first manifested in humans in November 2002. The SARS-associated coronavirus (SARS-CoV) has been identified as the causal agent, but the pathology and pathogenesis are still not quite clear.

PubMed: 16536279


Affiliations:


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pubmed:16536279

Le document en format XML

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<term>Middle Aged</term>
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<term>Antigènes CD (métabolisme)</term>
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<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Virus du SRAS (isolement et purification)</term>
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<term>Alvéoles pulmonaires</term>
<term>Fibrose pulmonaire</term>
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<term>Syndrome respiratoire aigu sévère</term>
<term>Épithélium</term>
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<term>Severe Acute Respiratory Syndrome</term>
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<term>SARS Virus</term>
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<term>Virus du SRAS</term>
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<front>
<div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is an emerging infectious disease that first manifested in humans in November 2002. The SARS-associated coronavirus (SARS-CoV) has been identified as the causal agent, but the pathology and pathogenesis are still not quite clear.</div>
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<DateCompleted>
<Year>2007</Year>
<Month>06</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised>
<Year>2016</Year>
<Month>08</Month>
<Day>18</Day>
</DateRevised>
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<ISSN IssnType="Print">0529-5807</ISSN>
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<Volume>34</Volume>
<Issue>10</Issue>
<PubDate>
<Year>2005</Year>
<Month>Oct</Month>
</PubDate>
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<Title>Zhonghua bing li xue za zhi = Chinese journal of pathology</Title>
<ISOAbbreviation>Zhonghua Bing Li Xue Za Zhi</ISOAbbreviation>
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<ArticleTitle>[Lung pathology and pathogenesis of severe acute respiratory syndrome: a report of six full autopsies].</ArticleTitle>
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<MedlinePgn>656-60</MedlinePgn>
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<Abstract>
<AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Severe acute respiratory syndrome (SARS) is an emerging infectious disease that first manifested in humans in November 2002. The SARS-associated coronavirus (SARS-CoV) has been identified as the causal agent, but the pathology and pathogenesis are still not quite clear.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Post-mortem lung samples from six patients who died from SARS from April to July 2003 were studied by light and electron microscopy, Masson trichromal staining and immunohistochemistry. Evidence of infection with the SARS-CoV was determined by reverse-transcription PCR (RT-PCR) , serological examination and electron microscopy.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Four of six patients had serological and RT-PCR evidence of recent infection of SARS-CoV. Morphologic changes are summarized as follows: (1) Diffuse and bilateral lung consolidation was seen in all patients (6/6) with increasing lung weight. (2) Diffuse alveolar damage was universal (6/6) with hyaline membrane formation (6/6), intra-alveolar edema/hemorrhage (6/6), fibrin deposition (6/6), pneumocyte desquamation (6/6). A marked disruption in the integrity of the alveolar epithelium was confirmed by immunostaining for the epithelial marker AE1/AE3 (6/6). (3) Type II pneumocytes, with mild hyperplasia, atypia, cytomegaly with granular amphophilic cytoplasm and intracytoplasmic lipid accumulation (5/6). (4) Giant cells in the alveoli were seen in five of 6 patients (5/6) , most of which were positive for the epithelial marker AE1/AE3 (5/6), but some cells were positive for the macrophage marker CD68(2/6). (5) A pronounced increase of macrophages were seen in the alveoli and the interstitium of the lung (6/6), which was confirmed by histological study and immunohistochemistry. (6) Haemophagocytosis was present in five of the 6 patients(5/6). (7) Lung fibrosis was seen in five patients(5/6), with alveolar septa and interstitium thickening(5/6), intraalveolar organizing exudates (6/6) and pleura thickening (4/6). Proliferation of collagen was confirmed by Masson trichromal staining, most of which was type III collagen by immunostaining. The formation of distinctive fibroblast/myofibroblast foci was seen in five patients (5/6) by light microscopy and immunochemistry. (8) Squamous metaplasia of bronchial mucosa was seen in five patients(5/6). (9) Thrombi was seen in all patients(6/6). (10) Accompanying infection was present in two patients, one was bacteria, the other was fungus. In addition, electron microscopy revealed viral particles in the cytoplasm of alveolar epithelial cells and endothelial cells corresponding to coronavirus.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Direct injury of SARS-CoV on alveolar epithelium, prominent macrophage infiltration and distinctive fibroblast/myofibroblast proliferation may play major roles in the pathogenesis of SARS.</AbstractText>
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