Antibody to severe acute respiratory syndrome (SARS)-associated coronavirus spike protein domain 2 cross-reacts with lung epithelial cells and causes cytotoxicity

Y. S. Lin, C. F. Lin, Y. T. Fang, Y. M. Kuo, P. C. Liao, T. M. Yeh, K. Y. Hwa, C. C K Shieh, J. H. Yen, H. J. Wang, I. J. Su, H. Y. Lei

Research output: Contribution to journalArticle

19 Citations (Scopus)


Both viral effect and immune-mediated mechanism are involved in the pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection. In this study, we showed that in SARS patient sera there were autoantibodies (autoAbs) that reacted with A549 cells, the type-2 pneumocytes, and that these autoAbs were mainly IgG. The autoAbs were detectable 20 days after fever onset. Tests of non-SARS-pneumonia patients did not show the same autoAb production as in SARS patients. After sera IgG bound to A549 cells, cytotoxicity was induced. Cell cytotoxicity and the anti-epithelial cell IgG level were positively correlated. Preabsorption and binding assays indicated the existence of cross-reactive epitopes on SARS-CoV spike protein domain 2 (S2). Furthermore, treatment of A549 cells with anti-S2 Abs and IFN-γ resulted in an increase in the adherence of human peripheral blood mononuclear cells to these epithelial cells. Taken together, we have demonstrated that the anti-S2 Abs in SARS patient sera cause cytotoxic injury as well as enhance immune cell adhesion to epithelial cells. The onset of autoimmune responses in SARS-CoV infection may be implicated in SARS pathogenesis.

Original languageEnglish
Pages (from-to)500-508
Number of pages9
JournalClinical and Experimental Immunology
Issue number3
Publication statusPublished - Sep 2005
Externally publishedYes



  • Autoantibody
  • Cytotoxicity
  • Lung epithelial cell
  • SARS
  • Spike protein

ASJC Scopus subject areas

  • Immunology

Cite this