SrasV1, PubMed, Curation, bibRecord, 001C78

SARS-CoV replicates in primary human alveolar type II cell cultures but not in type I-like cells.

Identifieur interne : 001C78 ( PubMed/Curation ); précédent : 001C77; suivant : 001C79

SARS-CoV replicates in primary human alveolar type II cell cultures but not in type I-like cells.

Auteurs : Eric C. Mossel [États-Unis] ; Jieru Wang ; Scott Jeffers ; Karen E. Edeen ; Shuanglin Wang ; Gregory P. Cosgrove ; C Joel Funk ; Rizwan Manzer ; Tanya A. Miura ; Leonard D. Pearson ; Kathryn V. Holmes ; Robert J. Mason

Source :

Virology [ 0042-6822 ] ; 2008.

RBID : pubmed:18022664

Descripteurs français

KwdFr :
- ARN viral (analyse), Alvéoles pulmonaires (cytologie), Alvéoles pulmonaires (virologie), Cellules cultivées, Différenciation cellulaire, Effet cytopathogène viral, Humains, RT-PCR, Réplication virale, Virologie (), Virus du SRAS (génétique), Virus du SRAS (physiologie), Épithélium (virologie).
MESH :
- analyse : ARN viral.
- cytologie : Alvéoles pulmonaires.
- génétique : Virus du SRAS.
- physiologie : Virus du SRAS.
- virologie : Alvéoles pulmonaires, Épithélium.
- Cellules cultivées, Différenciation cellulaire, Effet cytopathogène viral, Humains, RT-PCR, Réplication virale, Virologie.

English descriptors

KwdEn :
- Cell Differentiation, Cells, Cultured, Cytopathogenic Effect, Viral, Epithelium (virology), Humans, Pulmonary Alveoli (cytology), Pulmonary Alveoli (virology), RNA, Viral (analysis), Reverse Transcriptase Polymerase Chain Reaction, SARS Virus (genetics), SARS Virus (physiology), Virology (methods), Virus Replication.
MESH :
- chemical , analysis : RNA, Viral.
- cytology : Pulmonary Alveoli.
- genetics : SARS Virus.
- methods : Virology.
- physiology : SARS Virus.
- virology : Epithelium, Pulmonary Alveoli.
- Cell Differentiation, Cells, Cultured, Cytopathogenic Effect, Viral, Humans, Reverse Transcriptase Polymerase Chain Reaction, Virus Replication.

Abstract

Severe acute respiratory syndrome (SARS) is a disease characterized by diffuse alveolar damage. We isolated human alveolar type II cells and maintained them in a highly differentiated state. Type II cell cultures supported SARS-CoV replication as evidenced by RT-PCR detection of viral subgenomic RNA and an increase in virus titer. Virus titers were maximal by 24 h and peaked at approximately 10(5) pfu/mL. Two cell types within the cultures were infected. One cell type was type II cells, which were positive for SP-A, SP-C, cytokeratin, a type II cell-specific monoclonal antibody, and Ep-CAM. The other cell type was composed of spindle-shaped cells that were positive for vimentin and collagen III and likely fibroblasts. Viral replication was not detected in type I-like cells or macrophages. Hence, differentiated adult human alveolar type II cells were infectible but alveolar type I-like cells and alveolar macrophages did not support productive infection.

DOI: 10.1016/j.virol.2007.09.045
PubMed: 18022664

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is a disease characterized by diffuse alveolar damage. We isolated human alveolar type II cells and maintained them in a highly differentiated state. Type II cell cultures supported SARS-CoV replication as evidenced by RT-PCR detection of viral subgenomic RNA and an increase in virus titer. Virus titers were maximal by 24 h and peaked at approximately 10(5) pfu/mL. Two cell types within the cultures were infected. One cell type was type II cells, which were positive for SP-A, SP-C, cytokeratin, a type II cell-specific monoclonal antibody, and Ep-CAM. The other cell type was composed of spindle-shaped cells that were positive for vimentin and collagen III and likely fibroblasts. Viral replication was not detected in type I-like cells or macrophages. Hence, differentiated adult human alveolar type II cells were infectible but alveolar type I-like cells and alveolar macrophages did not support productive infection.</div>
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<Abstract><AbstractText>Severe acute respiratory syndrome (SARS) is a disease characterized by diffuse alveolar damage. We isolated human alveolar type II cells and maintained them in a highly differentiated state. Type II cell cultures supported SARS-CoV replication as evidenced by RT-PCR detection of viral subgenomic RNA and an increase in virus titer. Virus titers were maximal by 24 h and peaked at approximately 10(5) pfu/mL. Two cell types within the cultures were infected. One cell type was type II cells, which were positive for SP-A, SP-C, cytokeratin, a type II cell-specific monoclonal antibody, and Ep-CAM. The other cell type was composed of spindle-shaped cells that were positive for vimentin and collagen III and likely fibroblasts. Viral replication was not detected in type I-like cells or macrophages. Hence, differentiated adult human alveolar type II cells were infectible but alveolar type I-like cells and alveolar macrophages did not support productive infection.</AbstractText>
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   |texte=   SARS-CoV replicates in primary human alveolar type II cell cultures but not in type I-like cells.
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SARS-CoV replicates in primary human alveolar type II cell cultures but not in type I-like cells.

SARS-CoV replicates in primary human alveolar type II cell cultures but not in type I-like cells.

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