Abstract
Both well-known basic cellular and humoral factors of the adaptive antiviral immune response, which play an important role in the effectiveness of immunological reactions to inhibit viral infections, and new factors with which the efficiency of the functioning of cellular and humoral mechanisms of a specific immune response is associated are considered. This is, first of all, the presence of naive T-lymphocytes in the macroorganism, programmed to recognize a specific viral antigen. In addition, this is facilitated by various receptor specificities of T-lymphocytes, of which there are more than 20 million. The diversity of receptor structures was believed to be associated with the functioning of genes that activate recombinase. The development of antiviral cell-mediated mechanisms depends on interleukins 12, interferon-, and the transcriptional activator T-bet. An imbalance in the ratio of T-helper cell types 1 and 2 can lead to memory cell damage. Th-17 plays a central role in controlling the immune response to viral infection. The balance between activated cytotoxic CD-8+/T-helper cells and T-regulatory lymphocytes determines the risk of immunopathology. An excess of effector cells leads to immune-mediated damage, a lack of chronicity of a viral infection. One of the controlling mechanisms that ensure minimal damage to cells and tissues is the assembly of a cytoplasmic protein complex in antigen-presenting cellsinflammasomes. The intensity of inflammatory processes depends on whether the virus is cytopathic. The effectiveness of the humoral immune response is also attributed to the fact that one plasma cell can secrete more than 2,000 antibody molecules per second. One of the powerful properties of the adaptive antiviral immune response is the development of immunological memory by different types of memory T cells. To date, at least three subpopulations of memory T cells with different activation requirements have been identified. Thus, determining how each of these types of memory T-lymphocytes contributes to the long-term antiviral protection of the macroorganism is an urgent task.