Complement activation by respiratory syncytial virus-infected cells.
Respiratory syncytial virus (RSV), a major respiratory pathogen of children, has been speculated to cause disease by immunologic mechanisms. Although circulating levels of complement (C) are normal during RSV infections, the role of C in respiratory tract secretion is unclear. Since epithelial cells of the respiratory tract of children infected with RSV express viral surface antigens, the ability of RSV infected human cells to activate C was studied. RSV infected human cells (HeLa) were found to activate both the classical and alternative C pathways as measured by the cleavage of native C3 into its breakdown products. Increased C activation occurred in the presence of antibody. Cytolysis of RSV infected cells was then studied using a chromium release assay. Both the classical and alternative C pathways in the presence of antibody participated in the lysis of RSV infected cells. The combined effects of activation of C and the lysis of RSV infected cells by C and antibody may contribute to the pathogenesis of disease.
D000914:Antibodies, Viral / Q000032:analysis / Q000276:immunology; D000920:Antibody-Dependent Cell Cytotoxicity; D003167:Complement Activation; D003165:Complement System Proteins / Q000276:immunology; D003470:Culture Media; D006367:HeLa Cells; D006801:Humans; D012136:Respiratory Syncytial Viruses / Q000276:immunology; D010253:Respirovirus Infections / Q000276:immunology*
D000914:Antibodies, Viral; D003470:Culture Media; D003165:Complement System Proteins