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Tissue and cellular tropism of the coronavirus associated with severe acute respiratory syndrome: an in-situ hybridization study of fatal cases.

Authors
  • To, K F1
  • Tong, Joanna H M
  • Chan, Paul K S
  • Au, Florence W L
  • Chim, Stephen S C
  • Chan, K C Allen
  • Cheung, Jo L K
  • Liu, Esther Y M
  • Tse, Gary M K
  • Lo, Anthony W I
  • Lo, Y M Dennis
  • Ng, H K
  • 1 Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong SAR, China. [email protected] , (China)
Type
Published Article
Journal
The Journal of Pathology
Publisher
Wiley
Publication Date
Feb 01, 2004
Volume
202
Issue
2
Pages
157–163
Identifiers
PMID: 14743497
Source
Medline
Language
English
License
Unknown

Abstract

Severe acute respiratory syndrome (SARS) is a new human infectious disease with significant morbidity and mortality. The disease has been shown to be associated with a new coronavirus (SARS-CoV). The clinical and epidemiological aspects of SARS have been described. Moreover, the viral genome of SARS-CoV has been fully sequenced. However, much of the biological behaviour of the virus is not known and data on the tissue and cellular tropism of SARS-CoV are limited. In this study, six fatal cases of SARS were investigated for the tissue and cellular tropism of SARS-CoV using an in-situ hybridization (ISH) technique. Among all the tissues studied, positive signals were seen in pneumocytes in the lungs and surface enterocytes in the small bowel. Infected pneumocytes were further confirmed by immunofluorescence-fluorescence in-situ hybridization (FISH) analysis. These results provide important information concerning the tissue tropism of SARS-CoV, which is distinct from previously identified human coronaviruses, and suggest the possible involvement of novel receptors in this infection. Whereas the lung pathology was dominated by diffuse alveolar damage, the gut was relatively intact. These findings indicated that tissue responses to SARS-CoV infection are distinct in different organs. Copyright 2004 John Wiley & Sons, Ltd.

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