The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published online October 8, 2007
doi:10.1084/jem.20070462
The Journal of Experimental Medicine, Vol. 204, No. 11, 2529-2536
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Chen et al.
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BRIEF DEFINITIVE REPORT

 A novel subset of putative stem/progenitor CD34+Oct-4+ cells is the major target for SARS coronavirus in human lung

Yongxiong Chen1,4, Vera Sau-Fong Chan1,4, Bojian Zheng2, Kelvin Yuen-Kwong Chan3, Xiaoning Xu6, Leo Yuk-Fai To1,4, Fang-Ping Huang5, Ui-Soon Khoo3, and Chen-Lung Steve Lin1,4

1 Department of Surgery, 2 Department of Microbiology, and 3 Department of Pathology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China
4 Division of Surgery, Oncology, Reproductive Biology and Anaesthetics, Faculty of Medicine, and 5 Department of Molecular Genetics and Rheumatology, Division of Medicine, Imperial College London, Hammersmith Hospital, London W12 0NN, UK
6 Human Immunology Unit, The Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK

CORRESPONDENCE Chen-Lung Steve Lin: steve.lin{at}imperial.ac.uk

Identification of the nature of severe acute respiratory syndrome (SARS)-infected cells is crucial toward understanding the pathogenesis. Using multicolor colocalization techniques, we previously reported that SARS+ cells in the lung of fatally infected patients expressed the only known functional receptor, angiotensin-converting enzyme 2, and also a binding receptor, liver/lymph node–specific ICAM-3–grabbing non-integrin (CD209L). In this study, we show that SARS-infected cells also express the stem/progenitor cell markers CD34 and Oct-4, and do not express cytokeratin or surfactant. These putative lung stem/progenitor cells can also be identified in some non-SARS individuals and can be infected by SARS-coronavirus ex vivo. Infection of these cells may contribute to the loss of lung repair capacity that leads to respiratory failure as clinically observed.

Y. Chen and V.S.-F. Chan contributed equally to this work.


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