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As many as 97 patients with myocardial lesions: congestive and hypertrophic cardiomyopathy (CMP), postmyocarditis CMP (PM CMP), myocarditis (MC), alcoholic heart injury (AHI), coronary heart disease (CHD), vegetodysovarian myocardiodystrophy were examined by means of a complex of the virological tests (for Coxsackie B, Epstein-Barr and hepatitis B viruses) and immunoassays (for antibodies to different components of the myocardium, leukocyte migration inhibition test, antibody-dependent cellular cytotoxicity test, measurements of T and B lymphocytes and their subpopulations, and so forth). Virus infection was shown to be of a role for the onset of acute MC (usually reversible) and congestive CMP. At the same time the autoimmune mechanisms of the lesions were conclusively ascertained in MC associated with heart failure and in PM CMP. In patients with congestive CMP and AHI coupled with heart failure, antibodies to nerve fibers of the myocardium could be demonstrated in the presence of T-lymphocyte deficiency and high titers of antibodies to Epstein-Barr virus. This does not allow excluding myocardial denervation leading to refractory heart failure. Some immunological parameters made use of in the study provide an opportunity of an objective evaluation of the effect glucocorticoid treatment produces on patients suffering from MC and PM CMP.

Altogether 15 untreated patients aged 16 to 55 with diffuse toxic goiter had morphologically confirmed diagnosis of the presence of antibodies to Coxsackie virus (group B); titers of group A (1:128 and more) were revealed in 3 of them. It indicated recent (not more than 2 yrs.) Coxsackie virus infection. Such titers were absent in the control group (18 healthy persons). Difference in the study and control groups was statistically significant (p less than 0.05). The role of Coxsackie virus in the breakdown of natural tolerance to autologous thyroid tissue was discussed.

The paper presents the results of experimental infection of monkeys with virus-containing specimens from a patient with fecal-oral non-A-non-B hepatitis; the study was aimed at the determination of the possibilities of simulating this infection. Of the 8 monkeys infected with the material containing virus particles of fecal-oral non-A-non-B hepatitis 5 monkeys developed the infection manifested in virus excretion in fecal specimens, a rise in the level of serum aminotransferases, and typical histological lesions of the liver tissue. The infection could also be produced by inoculation of monkeys with virus-containing material from monkey. The above results indicate that the virus isolated from a human suffering from fecal-oral non-A-non-B hepatitis may induce in experimentally infected Macaca fascicularis monkeys a pathological process simulating viral hepatitis.

Four strains of ECHO-19 virus were isolated from a child with respiratory disease complicated with uveitis. A freshly isolated Rad/40 strain of ECHO-19 virus was found to produce a severe disease of the vascular coat of the eye (uveitis) in Javan Cercopithecus monkeys inoculated directly into the anterior chamber of the eye. Experimental uveitis is characterized by marked changes in the shape of the pupil, the lack of the pupil reaction to light, development of synechias, changes in the color of the iris. No uveitis developed after inoculation of the monkeys with the prototype Burke strain of ECHO-19 virus of culture fluid from uninoculated RD cell cultures (control). It is suggested that the freshly isolated strains of ECHO-19 virus (Rad/40 strain) could cause uveitis in the child under observation.

The results of neurological, pathomorphological and clinic-genealogical studies of vilyuisk encephalitis (VE), a chronic progressive disease of CNS, are presented. The disease is spread in Yakutija in Vilyui river basin (mainly in Vilyuisk and Kobyaisk regions) exclusively among native population and is known there since the middle of the last century. The results obtained suggest that VE (despite the existing opinion on its natural-focal virus etiology) is an ethnic hereditary disease with autosomal recessive type of transmission, is spread in a limited Yakut population by an ancestor effect and gradually gets out of the limits of this population at the expense of migration. According to its clinical symptoms and pathomorphological substrate of this main neurological syndrome (peculiar lower spastic paraparesis as a result of systemic ascending degeneration of lateral corticospinal tract of spinal cord), VE belongs to hereditary heterogenous group of diseases which are referred to Strümpell's spastic paraplegia. VE is different from the diseases of this group by the occurrence of cases with very rapid progressing and characteristic brain damages. To prevent further VE accumulation, it is necessary to concentrate efforts on biochemical and neurological studies in search of reliable tests for early detection of heterozygotes. Taking into account the hereditary nature of VE, its ethnic limitations and nosological self-dependence, it is expedient to designate the disease by its local name "bokhoroor".

A case of spontaneous hepatitis was detected in experiments aimed at working out the conditions for reproduction of the immunosuppressed state in Macaca fascicularis with the purpose of subsequent infection of these monkeys with non A non B hepatitis virus transmitted by the fecal-oral route. One of 6 monkeys at the 8th day of the experiment was found to have developed an increase in the level of serum aminotransferases which grew progressively reaching high values by day 14. Fecal specimens from this monkey collected on the 5th day and later contained spherical virus-like structures 27 nm in diameter, antigenically identical with hepatitis A (HAV) virus. In the other 5 monkeys, no similar structures were found in fecal specimens throughout the experiment. The monkey with the signs of hepatitis was sacrificed on the 16th day of experiment, i. e. on the 8th day from the onset of hyperenzymemia. Immune electron microscopy of extracts of hepatic tissue and fecal specimens collected from this monkey has revealed 27 nm particles antigenically identical with HAV. The bulk of viral particles from the liver sedimented in cesium chloride buoyant density zone of 1.32 g/cm3, and from fecal specimens in the zone of 1.36 g/cm3. In the liver of this monkey, histological changes were found which are observed in acute hepatitis, and HAV antigen in hepatocyte cytoplasm was detected by the fluorescent antibody technique. It is suggested that the spontaneous disease of this monkey was due to natural infection with HAV which could be provoked by experimental immunosuppression.

Strains of poliomyelitis, ECHO-11 and Coxsackie A7 viruses have first been shown to produce uveitis and keratouveitis in Javan macaca and green monkeys inoculated intraocularly. The most marked clinical picture of the eye affection in monkeys (keratoleukoma and opacity of the anterior chamber humor, edema and hyperemia of the iris, significant changes in the iris colour, development of posterior synechias, marked dilation of the pupil to 5-7 mm, no pupil reaction to light) was observed after inoculation with virulent strains of poliomyelitis virus types I, II, and III, and strains of ECHO-11 virus isolated from children with acute infectious uveitis. Uveitis symptoms in monkeys appeared within 20 hours after virus inoculation and persisted for 3 months of observation. No affection of the eyes developed after administration of flaviviruses or control material. In favour of freshly isolated strains of ECHO-11 virus being the cause of uveitis in the children examined are the following facts: ECHO-11 virus was isolated from 5 out of 10 children with uveitis, neutralizing antibody to ECHO-11 virus was found in 8 out of 9 children with uveitis, seven of them showing a rise in antibody titres to ECHO-11 virus to 1:256-1:1024, the clinical picture of uveitis reproduced in monkeys is very similar to that of uveitis in children. The potential role of poliomyelitis viruses and other enteroviruses in the etiology of human uveitis is discussed.

A model of persistent infection with Coxsackie B-3 virus was developed in adult mice with clinical manifestations of the disease and long-term (up to 13 months) excretion of the causative agent. The method of multiple organ cultures was shown to be suitable for isolation of the persisting enterovirus. The presence of persistent infection was confirmed by the detection of IgM antibody in repeated daily examinations of the animals for 4 months. It seems to be expedient to use this model for investigations of the pathogenesis and methods of treatment of persistent Coxsackie B-3 infection in experimental animals.

In order to prevent the unfavourable effect of weightlessness, it is recommended to use individual suits for long wear. These include a preventive pressure suit which provides an axial pressure on the skeleton and moments of forces during movement, and a preventive vacuum suit which provides lower body decompression. The suits ensures the conditions for the function of the musculoskeletal apparatus and the cardiovascular system which are close to those on the Earth.

Typical acute hepatitis was reproduced in a human volunteer immune to hepatitis A virus (HAV) after oral administration of pooled stool extracts from presumed cases of epidemic non-A, non-B hepatitis. Markers of hepatitis B infection, anti-HAV IgM, and increase in total anti-HAV level were not detectable in the volunteer's sera during the course of infection. Spherical 27- to 30-nm virus-like particles were visualized by immune electron microscopy (IEM) in stool samples collected during preclinical and early postclinical phases. These particles banded in CsCl at a buoyant density of 1.35 g/cm3. They reacted in the IEM test with sera from individuals who had experienced two non-B hepatitis episodes but did not react with sera from routine anti-HAV IgM-positive hepatitis patients. Intravenous inoculation of cynomolgus monkeys with the virus-containing stool extract resulted in histopathologically and enzymatically confirmed hepatitis, excretion of virus-like particles, and antibody response to them.

Circulation of a virus similar to human hepatitis A virus by antigenic and some other properties was observed among African green monkeys imported from their natural habitats. In some of the monkeys this virus caused a disease similar to hepatitis A in many features.