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Objective: To compare clinical characteristics in children with enterovirus infections (EVI) and meningitis with detailed characteristics of the changes in the content of cerebrospinal fluid (CSF) confirmed in the laboratory., Material and Methods: The results of examinations of 97 children, aged from 2.5 to 15 years, 3 adolescents and 1 adult female patient with EVI were analyzed. Enterovirus RNA isolation and detection in feces and CSF was performed using PCR., Results and Conclusion: Enterovirus RNA in CSF was detected in 44 children, including 3 patients with cytosis (5-7-19 cells in 3 mm3). The frequency and severity of symptoms in 42 patients with EVI and meningitis, 14 children with EVI without meningitis and 8 patients with ICD-10 «Meningitis unspecified» are presented. The initial CSF pleocytosis in 1-3 day (4-5 day for two-wave course) in EVI and meningitis was <100 in 4, from 100 to 1000 in 33, >1000 (max 3036) cells in 3 mm3 in 5 patients, including 15 with the predominance of neutrophils (from 77 to 97% in cytosis 114-2300 cells in 3 mm(3)). In the peripheral blood, leukocytosis 10.9-13.8×10(9)/л was noted in 12 children and leukocytosis 14.4-18.7×10(9)/л with the «left shift» in 7. Most of the children (n=37) with EVI and meningitis were discharged from the hospital within 10-17 days. The authors suggest the importance of including the variety of clinical presentations of EVI in the additional item «B10 Enterovirus infections» in upcoming ICD-11.

Antigens of enteroviruses were detected quantitatively in the modified complement-binding reaction in blood samples from 102 of the 208 (49%) patients with ACS, in coronary artery tissues from 23 of 24 and heart from 51 of 94 (54.3%) patients with MI who died from cardiogenic shock and/or cardiac rupture. The relative level of enterovirus antigen (RLEVA) in the blood of patients with MI complicated and uncomplicated by cardiogenic shock and/or cardiac rupture was 0.42 +/- 0.04 and 0.29 +/- 0.02 arbitrary units respectively (p = 0.032) compared with 0.21 +/- 0.07 in patients with unstable angina (UA) (p = 0.0001). RLEVA in patients with UA was significantly lower than in those with uncomplicated MI (p < 0.011). RLEVA in necrotized myocardial areas after death from cardiogenic shock (0.54 +/- 0.18) and/or cardiac rupture (0.46 +/- 0.15) was higher than outside MI zones (0.30 +/- 0.14 and 0.26 +/- 0.10 respectively) (p < 0.01). RLEVA in coronary vessels feeding the necrotic zones of patients with MI complicated by cardiogenic shock (0.44 +/- 0.18) was higher (p = 0.03) than in the vessel feeding tissues outside the MI zone (0.29 +/- 0.19). It is concluded that enterovirus infection is a factor of ACS; it is directly involved in its pathogenesis and promotes the development of cardiogenic shock and/or cardiac rupture.

Effects of viruses and bacterial associations are suggested to promote secondary purulent intracranial complications in ENT patients. Fundamental aspects of pathogenesis of viral neuroinfections and pathogenetic mechanisms of different conditions provoked by viral factors promoting bacterial complications are presented. Hemoculture, and cerebrospinal fluid in 24 patients with secondary purulent rhinogenic and otogenic meningitis were studied with polymerase chain reaction for enteroviruses, cytomegaloviruses, Epstein-Barr, herpes, zoster viruses. The viruses were present in the studied media in 29.4% samples.

Molecular hybridization studies have demonstrated that human enteroviruses, including group B coxsackieviruses (CVB), are detectable in myocardial tissue of patients with acute and chronic myocarditis. As well, such infections are observed in some patients with end-stage dilated cardiomyopathy indicating the possibility of persistent heart muscle infection. Enterovirus persistence in the human heart is supported by the discovery in various murine models of chronic myocarditis, demonstrating that coxsackievirus B3 (CVB3), typically a cytolytic virus, is capable of evading immunological surveillance in a host-dependent manner. Currently attention is focused on the analysis of molecular mechanisms of virus persistence, the characterization of viral and host factors and their impact in determining the natural course of myocardial enterovirus infections. The evidence for a causal linkage of enterovirus infection with heart muscle diseases has emerged therapeutic implications. From the view of a virologist, immunosuppressive treatment of patients revealing enterovirus infection in the myocardium with steroids is clearly contraindicated. The evaluation of potent antiviral agents, such as interferons, in established in vitro and in vivo model systems of enterovirus infection is expected to contribute significantly to new therapeutic strategies in human enteroviral heart disease.

An analysis is presented of CT examination of the brain in viral meningoencephalitis in 113 patients with viral encephalitis. Pathological changes in the acute period were found in 65.4% of patients more frequently in the CSF system, rarer in the brain tissue (in herpetic encephalitis). During the early convalescence period 75% of patients showed dilated ventricles and external CSF spaces. The importance of CT examination in this kind of pathology is emphasized.

A total of 224 cases with endogenic uveitis in infants are analyzed. The results of complex clinical and immunological analysis and serologic findings bring the authors to a conclusion that enteroviral uveitis makes up 42 percent of all uveitis in children aged under 3 and that this condition is prevalent in this country. Typical late complications, long persistence of virus-neutralizing antibodies in high titers (up to 8-10 years after convalescence) permit a retrospective etiological diagnosis.

Brain neurosonography was performed in 15 babies with toxicosis-+-linked nervous disorders. Three types of the brain structure were established in the patients: 1, marked brain swelling in all patients; 2, concomitant perinatally induced brain structures' changes; 3, intracranial hemorrhage focuses resulting from the DIC syndrome. The technique is useful for precise diagnosis and prognosis of the outcome of the neurotoxic coma.

Reproduction of mouse encephalomyocarditis virus (EMC) was studied in 5 continuous primate cell lines: HeLa, Fl, Detroit-6, P/7, and MIO inoculated with guanidine-dependent variant of poliomyelitis virus in the absence of guanidine. Poliomyelitis virus stimulated EMC virus reproduction in all cell lines under study. This stimulation effect was studied at length in HeLa and MIO cells. In HeLa cells, stimulation was observed at a low and moderate multiplicity of infection of EMC virus but not at a high (100 PEU/cell) multiplicity. Also, when EMC virus reproduction was stimulated, a shortening of the latent period of its multiplication cycle, an increase in the number of antigen-containing cells and the number of infectious centers were observed. In MIO cells, stimulation was found to occur both with low and high doses of EMC virus but not to be accompanied by a shortening in the latent period of EMC reproduction cycle, or any increase in the antigen-containing cells or number of infectious centers. In both cell types upon mixed infection the synthesis of virus-specific RNA's of EMC virus was enhanced. It is suggested that the stimulating effect of poliomyelitis virus is realized in HeLa and MIO cells at different stages of EMC virus reproduction.