Main Article Content
When HCV and HBV infections interact with the immune system, both adaptive humoral reactions with the formation of specific antibodies and the production of cytokines are activated. In this case, the leading factor in the development of chronic viral hepatitis HBV, HCV is insufficient production of cytokines and / or a decrease in the sensitivity of viruses and body cells to them, which is possibly due to the influence of allelic variants of cytokine gene polymorphism [5,7].
In the developing focus of the inflammatory response in viral hepatitis, macrophages and T-lymphocytes mainly accumulate, which synthesize many proinflammatory cytokines, such as IL-1, IL-6, IFN-?, TNF-? and others . Various xenobiotics cause additional activation of the hepatic tissue, which, in turn, can lead to the launch of the entire cascade of the inflammatory response. This is accompanied by an imbalance of pro- and anti-inflammatory cytokines and impaired cell-cell interactions and expression of cytokine genes on immune cells.
Each cytokine gene and its receptor has up to 20 allelic variants, which differ mainly in their influence on the final level of cytokine production. Various combinations of allelic variants of cytokine genes can form both their balanced production, characteristic of two main groups of regulatory lymphocytes - Th1 and Th2, and unbalanced . In this case, an individual ensemble of allelic variants of cytokine genes can partially determine the nature of the inflammatory process, its course and outcomes [4, 6].
In this regard, the identification of "candidate genes" of chronic viral hepatitis HBV, HCV, mixed infections HBV + HCV, HBV + HDV and occult hepatitis with an outcome in LC, especially in accordance with population differences, can become the basis for predictive molecular prediction of individual predisposition and response to antiviral therapy.