INFLUENCE ON CELLULAR TARGETS FOR TREATING INFLUENZA INFECTION

Abstract

Аbstract. Influenza is a highly contagious infection of humans. The use of specific antivirals leads to emergence of drug-resistant strains following by the decrease of efficacy of ethiotropic chemotherapy. In this review the data about the decrease of the level of viral replication and severity of pathological process based on the use of alternative targets of cellular instead of viral origin are presented. The medicines for decreasing the production of proinflammatory cytokines (eritoran), restricting the degranulation of mast cells (ketotifen), inhibitors of cyclooxygenases (celexocib, mesalasine, SC-560), inhibitors of sphingosine-1-phospate pathway (AAL-R) and compounds increasing the capillars stability by strengthe ning the contacts between endothelial cells (Slit protein) have been described in the review. The special attention is paid to the inhibitors of cellular pathways that are used by the virus to provide its reproduction, such as NF-κB, Raf/MEK/ERK, PI3K/AKT/mTOR. Information concerning anti-influenza activity of kinase and autophagy inhibitors is summarised as well as data about the preparations of combined mechanism of activity — glycirrhizic acid and dipeptide alpha-glutamyl-tryptophane. Further studies in the field of search and optimization of inhibitors of cellular components as remedies against influenza infection could lead to the development of novel antivirals with high efficacy, broad spectrum of activity and low probability of virus resistance.

Keywords

• influenza
• host targets
• inflammation
• signal pathways
• antivirals