ATYPICAL CHRONIC ACTIVE HERPESVIRUS INFECTIONS: ETIOLOGICAL STRUCTURE, FREQUENCY OF OCCURRENCE, CLINICAL SYNDROMES ASSOCIATED WITH THEM

Abstract

Background: Every year, a steady, progressive increase in the number of atypical, chronic, active forms of infections caused by herpesviruses (AHA-HVI) is recorded. The diagnosis and selection of adequate therapeutic strategies for the treatment of these forms of infections presents significant difficulties for physicians of therapeutic, neurological profile, immunologists, infectious disease specialists, due to the polysyndromicity and the presence of many clinical masks of these infections. Aims: determining the prevalence of AHA-HVI among patients infected with herpes virus infections, as well as studying the features of the etiological structure and clinical manifestations/criterion signs of atypically occurring chronic forms of herpes viral infections. Materials and methods: Under our supervision at the Medsi CDC in Belorusskaya (Moscow) there were 98 patients (SG) of both sexes aged 23 to 60 years suffering from AHA-HVI. The comparison group consisted of 30 conditionally healthy subjects comparable in sex and age to SG patients. In addition to traditional methods (history collection, physical examination methods, CBC, etc.), serodiagnosis methods with ELISA were used to detect herpes-viral infections; PCR method for detecting the genome of viruses in biomaterials. The study was approved by the ethics committee, and all patients received informed consent to participate in the study. Statistical analysis was performed using adequate methods of statistic studies. Results: The study of the etiological structure of herpes virus infections in patients with AHA-HVI, mixed HVI was shown to occur in 83.4% of patients, and mono-HVI in 16.6% of cases. It was shown that EBV was the dominant virus among patients with both mono and mixed GVI. A high rate of EBV DNA detection was demonstrated in saliva (84.2%), posterior pharyngeal wall scraping (73.5%) and tonsils (42.9%), urine (12.6%) and blood (8.3%) is a marker of high replicative activity of the virus. The main clinical syndromes associated with the course of mono and mixed AHA-HVI were identified. Conclusions: Identification and quantitative assessment of the viral load associated with the severity of the course and severity of clinical manifestations of ACA-HVI, as well as clarification of the features of clinical manifestations and syndromes in patients suffering from various mono-, mixed-herpesvirus infections, allow us to outline goals for the further development of an adequate diagnostic algorithm for these atypical forms of herpesvirus infections and the concept of targeted, personalized etio- and immunopathogenetic therapy.