SrasV1, Ncbi, Merge, bibRecord, 001049

A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury.

Identifieur interne : 001049 ( Ncbi/Merge ); précédent : 001048; suivant : 001050

A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury.

Auteurs : Keiji Kuba [Autriche] ; Yumiko Imai ; Shuan Rao ; Hong Gao ; Feng Guo ; Bin Guan ; Yi Huan ; Peng Yang ; Yanli Zhang ; Wei Deng ; Linlin Bao ; Binlin Zhang ; Guang Liu ; Zhong Wang ; Mark Chappell ; Yanxin Liu ; Dexian Zheng ; Andreas Leibbrandt ; Teiji Wada ; Arthur S. Slutsky ; Depei Liu ; Chuan Qin ; Chengyu Jiang ; Josef M. Penninger

Source :

Nature medicine [ 1078-8956 ] ; 2005.

RBID : pubmed:16007097

Descripteurs français

KwdFr :
- Analyse de variance, Animaux, Carboxypeptidases (métabolisme), Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (génétique), Glycoprotéines membranaires (métabolisme), Immunohistochimie, Maladies pulmonaires (anatomopathologie), Maladies pulmonaires (enzymologie), Maladies pulmonaires (étiologie), Peptidyl-Dipeptidase A, Protéines de l'enveloppe virale (génétique), Protéines de l'enveloppe virale (métabolisme), Souris, Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (enzymologie), Virus du SRAS (génétique), Virus du SRAS (métabolisme).
MESH :
- anatomopathologie : Maladies pulmonaires.
- enzymologie : Maladies pulmonaires, Syndrome respiratoire aigu sévère.
- génétique : Glycoprotéines membranaires, Protéines de l'enveloppe virale, Virus du SRAS.
- métabolisme : Carboxypeptidases, Glycoprotéines membranaires, Protéines de l'enveloppe virale, Virus du SRAS.
- étiologie : Maladies pulmonaires.
- Analyse de variance, Animaux, Glycoprotéine de spicule des coronavirus, Immunohistochimie, Peptidyl-Dipeptidase A, Souris, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Analysis of Variance, Animals, Carboxypeptidases (metabolism), Immunohistochemistry, Lung Diseases (enzymology), Lung Diseases (etiology), Lung Diseases (pathology), Membrane Glycoproteins (genetics), Membrane Glycoproteins (metabolism), Mice, Peptidyl-Dipeptidase A, SARS Virus (genetics), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (complications), Severe Acute Respiratory Syndrome (enzymology), Spike Glycoprotein, Coronavirus, Viral Envelope Proteins (genetics), Viral Envelope Proteins (metabolism).
MESH :
- chemical , genetics : Membrane Glycoproteins, Viral Envelope Proteins.
- chemical , metabolism : Carboxypeptidases, Membrane Glycoproteins, Viral Envelope Proteins.
- complications : Severe Acute Respiratory Syndrome.
- enzymology : Lung Diseases, Severe Acute Respiratory Syndrome.
- etiology : Lung Diseases.
- genetics : SARS Virus.
- metabolism : SARS Virus.
- pathology : Lung Diseases.
- Analysis of Variance, Animals, Immunohistochemistry, Mice, Peptidyl-Dipeptidase A, Spike Glycoprotein, Coronavirus.

Abstract

During several months of 2003, a newly identified illness termed severe acute respiratory syndrome (SARS) spread rapidly through the world. A new coronavirus (SARS-CoV) was identified as the SARS pathogen, which triggered severe pneumonia and acute, often lethal, lung failure. Moreover, among infected individuals influenza such as the Spanish flu and the emergence of new respiratory disease viruses have caused high lethality resulting from acute lung failure. In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor. The high lethality of SARS-CoV infections, its enormous economic and social impact, fears of renewed outbreaks as well as the potential misuse of such viruses as biologic weapons make it paramount to understand the pathogenesis of SARS-CoV. Here we provide the first genetic proof that ACE2 is a crucial SARS-CoV receptor in vivo. SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway. These results provide a molecular explanation why SARS-CoV infections cause severe and often lethal lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses.

DOI: 10.1038/nm1267
PubMed: 16007097

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 002651
to stream PubMed, to step Curation: 002651
to stream PubMed, to step Checkpoint: 002865

Links to Exploration step

pubmed:16007097

Le document en format XML

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<front><div type="abstract" xml:lang="en">During several months of 2003, a newly identified illness termed severe acute respiratory syndrome (SARS) spread rapidly through the world. A new coronavirus (SARS-CoV) was identified as the SARS pathogen, which triggered severe pneumonia and acute, often lethal, lung failure. Moreover, among infected individuals influenza such as the Spanish flu and the emergence of new respiratory disease viruses have caused high lethality resulting from acute lung failure. In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor. The high lethality of SARS-CoV infections, its enormous economic and social impact, fears of renewed outbreaks as well as the potential misuse of such viruses as biologic weapons make it paramount to understand the pathogenesis of SARS-CoV. Here we provide the first genetic proof that ACE2 is a crucial SARS-CoV receptor in vivo. SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway. These results provide a molecular explanation why SARS-CoV infections cause severe and often lethal lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses.</div>
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<Abstract><AbstractText>During several months of 2003, a newly identified illness termed severe acute respiratory syndrome (SARS) spread rapidly through the world. A new coronavirus (SARS-CoV) was identified as the SARS pathogen, which triggered severe pneumonia and acute, often lethal, lung failure. Moreover, among infected individuals influenza such as the Spanish flu and the emergence of new respiratory disease viruses have caused high lethality resulting from acute lung failure. In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor. The high lethality of SARS-CoV infections, its enormous economic and social impact, fears of renewed outbreaks as well as the potential misuse of such viruses as biologic weapons make it paramount to understand the pathogenesis of SARS-CoV. Here we provide the first genetic proof that ACE2 is a crucial SARS-CoV receptor in vivo. SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway. These results provide a molecular explanation why SARS-CoV infections cause severe and often lethal lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses.</AbstractText>
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A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury.

A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury.

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