The interrelation between specific and non-specific immunity in the pathogenesis of acute herpetic stomatitis

Abstract

Background. Acute herpetic stomatitis is accompanied by secondary immunodeficiency, associated with a functional insufficiency of cells, a decrease in their number or an imbalance of the components of the immune system. The study aims to describe the role of immunity in the evolution and manifestation of acute herpetic stomatitis. Materials and methods. A literature review used 45 scientific articles from PubMed, UpToDate, and NCBI, only works published in the last five years were selected. Results. In herpetic stomatitis, the body's non-specific protective factors are the first to interact with the viral agent. Tissue macrophages are the cells involved in the immune response to the penetration of the viral agent into the microorganism, participating in both the specific and non-specific immune response. These cells capture and engulf pathogens, presenting antigenic proteins to T and B lymphocytes, which initiate the development of cellular and humoral immune responses. Macrophages respond to viral invasion by rapidly producing anti-inflammatory cytokines due to activation of neutrophils, monocytes, macrophages, NK cells and W lymphocytes, including the specific immune response. The concept of "oral tolerance" is based on a complex system of interactions between oral microflora, immunological protection and non-specific barrier mechanisms. The subepithelial lymphoid tissue represents a protective barrier against the penetration of foreign agents. The primary role is attributed to a protein (lysozyme), which acts as a mucolytic enzyme. Conclusions. The state of the body's immune system plays a vital role in the clinical manifestation of HVS-1 infection, which influences the development of the infectious process in herpes infection by changing the proportions of viral components. The immune response of the microorganism is directed both against virus-infected cells and against the virus itself. It is determined by two defence mechanisms: specific immunity formed after the disease or artificial immunisation and natural resistance.