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The study outcomes are indicative of a relationship between periodontal lesions and persistent viral infection in the oral cavity tissues, which exacerbates the degree of severity of lesions.81 young children underwent examination and were assigned into three groups. The first group included 29 children who are commonly and chronically ill (sickly) (35.8%). The second study group included 30 HIV positive children (37.03%). The third control group included 22 children (27.16%) aged 1 to 6 years, who were found virtually healthy. Causation of the herpes simplex virus (HSV-1), the cytomegalovirus (CMV) and the Epstein-Barr virus (EBV) in the onset and development of the clinical presentation of the above lesions was determined by sampling of materials from the surfaces of lesion elements, followed by cytology and molecular and genetic studies with a view to detect DNA pathogens in the material collected.21 commonly and chronically ill (sickly) children have been defined as the herpes virus carriers (72.41%). The mixed persistent viral infection was found only in 14.29% of cases. Clinical manifestations of persistent viral infection in the oral mucosa were registered in 14 patients (48.27%) in Group 1.73.33% of children infected with HIV tested positive for carrier state of persistent viral infection, according to the research findings in Group 2, yet with a predominance of viral associations (59.09%), which were accompanied by the detection of mucous membrane lesions – in 93.3% of children. The growing degree of immunological changes in children with immunodeficiency disorders in both study groups preconditions the occurrence and progression of mucosal lesions associated with the herpes virus infection.Clinical manifestation of the CMV, HSV and EBV viruses in the examined children is clearly a presentation of secondary immunodeficiency disorders disrupting local immunity, causing changes in oral microbiota and development of catarrhal gingivitis and aphthous stomatitis, which is indicative of their unconditional role in the onset of the disorder and requires introduction of appropriate changes to the clinical practice guidelines by inclusion of antiviral and probiotic therapies.