Complement activation by respiratory syncytial virus-infected cells

Abstract

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.