Respiratory syncytial virus (RSV) is the most common pathogen of the lower respiratory tract in infants. Once RSV infection is established, the host immune response includes the production of virus-neutralising antibodies and T-cell-specific immunity. In addition, recent findings suggest that signaling through Toll-like receptor 4 (TLR4) has an important role in innate immunity to RSV. Acute RSV infection in infancy may produce some asthma-like symptoms and a recurrent wheeze may follow later in childhood, but the immunological mechanisms by which RSV contributes to the development of asthma are poorly understood. One of the prevailing theories posits indirect stimulation of the disease process via promotion of sensitisation to inhalant allergens, as a result of the intrinsically "Th2-trophic" effects of the virus. Experiments in mice and indirect evidence in humans suggest that this may be due to attenuated capacity of infants to mount systemic IFN- and IL-12 responses, resulting in generation of effector T cells that predominately secrete Th2 cytokines such as IL-4 and IL-13, which are also found in atopy and asthma. The gain-of-function variants of T helper type 2 cytokine genes may also play a role in increasing the severity of RSV disease. We showed previously that RSV infection increases the expression of B cell antigen CD23, a putative participant in Th2 responses, which was accompanied by RSV-specific IgE and IgG4 antibodies. Furthermore, others and we showed that in some infants RSV infection is associated with IL-4 production in peripheral T cells. Our more recent data demonstrated increased percentage of TLR4-expressing monocytes in some RSV infected infants. Further experiments are necessary in order to develop strategies for the prevention of RSV infection and its role in the subsequent development of persistent wheezing and asthma-like symptoms in childhood.

Temeljne medicinske znanosti,Kliničke medicinske znanosti