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Journal of Virology, March 2006, p. 2684-2693, Vol. 80, No. 6
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.6.2684-2693.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Modeling the Early Events of Severe Acute Respiratory Syndrome Coronavirus Infection In Vitro

Yu-Ting Yen,1 Fang Liao,2 Cheng-Hsiang Hsiao,3 Chuan-Liang Kao,4 Yee-Chun Chen,5 and Betty A. Wu-Hsieh1*

Graduate Institute of Immunology,1 Graduate Institute of Clinical Laboratory Sciences and Medical Biotechnology, National Taiwan University College of Medicine,4 Department of Pathology,3 Department of Internal Medicine, National Taiwan University Hospital,5 Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan2

Received 13 September 2005/ Accepted 15 December 2005

The clinical picture of severe acute respiratory syndrome (SARS) is characterized by pulmonary inflammation and respiratory failure, resembling that of acute respiratory distress syndrome. However, the events that lead to the recruitment of leukocytes are poorly understood. To study the cellular response in the acute phase of SARS coronavirus (SARS-CoV)-host cell interaction, we investigated the induction of chemokines, adhesion molecules, and DC-SIGN (dendritic cell-specific ICAM-3-grabbing nonintegrin) by SARS-CoV. Immunohistochemistry revealed neutrophil, macrophage, and CD8 T-cell infiltration in the lung autopsy of a SARS patient who died during the acute phase of illness. Additionally, pneumocytes and macrophages in the patient's lung expressed P-selectin and DC-SIGN. In in vitro study, we showed that the A549 and THP-1 cell lines were susceptible to SARS-CoV. A549 cells produced CCL2/monocyte chemoattractant protein 1 (MCP-1) and CXCL8/interleukin-8 (IL-8) after interaction with SARS-CoV and expressed P-selectin and VCAM-1. Moreover, SARS-CoV induced THP-1 cells to express CCL2/MCP-1, CXCL8/IL-8, CCL3/MIP-1{alpha}, CXCL10/IP-10, CCL4/MIP-1ß, and CCL5/RANTES, which attracted neutrophils, monocytes, and activated T cells in a chemotaxis assay. We also demonstrated that DC-SIGN was inducible in THP-1 as well as A549 cells after SARS-CoV infection. Our in vitro experiments modeling infection in humans together with the study of a lung biopsy of a patient who died during the early phase of infection demonstrated that SARS-CoV, through a dynamic interaction with lung epithelial cells and monocytic cells, creates an environment conducive for immune cell migration and accumulation that eventually leads to lung injury.

* Corresponding author. Mailing address: Graduate Institute of Immunology, College of Medicine, National Taiwan University, No. 1 Jen-Ai Road, Section 1, Taipei 10051, Taiwan. Phone: 886-2-23123456, ext. 8630. Fax: 886-2-23217921. E-mail: wuhsiehb{at}ha.mc.ntu.edu.tw.

Journal of Virology, March 2006, p. 2684-2693, Vol. 80, No. 6
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.6.2684-2693.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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