Modulation of respiratory syncytial virus receptors, TLR4 and CX3CR1 in children with bronchiolitis

Respiratory syncytial virus (RSV) is the leading cause of serious lower respiratory tract illness in infants and young children. Approximately 80% of childhood bronchiolitis cases and 50% of infant pneumonias are attributable to RSV infection. RSV fusion (F) protein, responsible for the merging of RSV infected with adjacent uninfected epithelial cells, also stimulates cytokine production in monocytes through CD14 and Toll-like receptor 4 (TLR4). Another surface glycoprotein, protein G, functionally mimics CX3C chemokine fractalkine, regulator of cytotoxic effector lymphocytes' tissue migration. It has been shown in mice that RSV G glycoprotein modifies cytokine and chemokine expression, sensitizes for pulmonary eosinophilia and alters pulmonary leukocyte trafficking. In our present study we analyzed the expression of perforin, IFN-?, IL-4 and fractalkine receptor CX3CR1 on cytotoxic T lymphocytes (n=11), and TLR4 expression on monocytes. The samples were obtained from peripheral blood of acutely ill infants with bronchiolitis (aged from 2 weeks to 5 months) and 4-6 weeks after the resolution of the disease. The observed effects of RSV infection on the above listed cytokines and receptor expression will be discussed.