engleski

Immunological reactivity to respiratory synytial virus (RSV) infestion

Respiratory syncytial virus (RSV) is common winter season respiratory pathogen that affects humans.Together with measles and mumps virus, RSV belongs to family of Paramyxoviridae, although it is less severe when it comes to disease severity and outcome. Today, RSV is the most frequent viral pathogen in infants causing lower respiratory tract infections whereas in adults, infection is localized to upper respiratory tract characterized by mild and transient inflammation. Infection in infants is often characterized by bronchiolitis and wheezing due to bronchiole mucus plugging and bronchoconstriction, which in some cases require hospitalization. Certain percentage of infants experience recurrent RSV infections and develop the airway hyperactivity that could result in development of allergic asthma later in childhood. There are many hypothesis on RSV caused pathology in infants ; immaturity of immune system, inadequate innate immune response or ability of the virus to circumvent effective adaptive anti-viral responses shifting from type 1 to type 2 immune responses, since some clinical symptoms of RSV bronchiolitis resemble to acute allergic asthmatic attack In our isnvestigation we confirmed that infants with acute RSV infection produce more IL-4 cytokine that correlates to disease severity. Predominance of type 2 response in acute RSV infection is not only accompanied by increased expression of the low affinity IgE receptor (CD23) but also the synthesis of specific anti-RSV IgE and IgG4 antibodies. Since innate immunity is part of immune system with ability to recognize and act upon pathogen challenge, importance of Toll-like receptors (TLR) that “ sense” RSV have major role in the control of viral replication and development of specific anti-viral response. Analyzing peripheral blood cells from infants with RSV infection, we found that extracellular TLR4 (recognizing RSV glycoprotein G) and intracellular TLR3, TLR7 and TLR8 (recognizing RSV RNA molecule) are expressed at lower level. Lower TLRs expression could relate with inadequate engagement in innate immunity mechanisms followed by the insufficient dendritic cell maturation and the lower adaptive cytokine synthesis.

RSV; inate immunity; toll-like receptors

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