Etiological therapy of respiratory-synchitic viral infection in the present and future

For several decades, acute respiratory infections caused by respiratory syncytial virus (RSV) have been a leading cause of respiratory tract pathology in young children. The aim is to highlight modern concepts of pathogenesis and the main directions of medicamentous treatment of respiratory syncytial virus infection. Two antigenic subtypes of RSV have been identified: A and B, and at least 37 genotypes of RSV type B and 13 genotypes of RSV type A. Respiratory syncytial virus infection (RSVI) in young children is characterized by a high probability of unfavorable life-threatening course, which requires hospitalization. Despite significant advances in virology and molecular biology that reveal the details of RSV interaction with the macrophage and the functioning of RSV replication mechanisms, treatment recommendations for patients with RSVI are limited mainly to pathogenetic and symptomatic therapy. Ribavirin, a nucleoside analog, is the only FDA-licensed antiviral agent for the treatment of RSVI that moderately inhibits viral replication. Instead, scientists are focusing on the development of new drugs that inhibit the activity of various viral proteins and surface receptor molecules of respiratory tract epithelial cells. The most promising drugs in this group are chemical compounds that inhibit RSV protein F, in particular, ziresovir, which is in phase III clinical trials. Currently, the possibility of using receptor tyrosine kinase inhibitors, such as erlotinib and vandetanib, in the treatment of RSVI is being investigated. Non-nucleoside inhibitors of RSV L-protein RNA polymerase, in particular the small molecule PC786, have great prospects for effective use in RSVI. It is also believed that the CX3CR1 receptor is the most promising target for drugs that will be developed to control the level of expression during the prevention and treatment of RSVI. The authors declare no conflict of interest.