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The authors studied the phenomenon of superhigh virulence for monkeys of viruses ECHO 11 (E11) and ECHO 19 (E19) isolated in 1981-1991 in Russia and Tadzhikistan from children with acute enterovirus uveitis or severe enterovirus infection. In 21 morphologically examined animals after coma, macrofocal or total necrosis of hepatocytes in weak inflammation was seen as early as experiment day 1-6. Hepatic lesion interpreted as hepatosis underlies acute hepatic failure with lethal outcome. The most intensive reproduction of viruses E11 and E19 occurred in the liver. Changes in the kidneys, lungs, spleen, adrenals, CNS detected in many animals aggravated the disease, but were not the primary cause of death. The disease in monkey was similar by the main criteria to superacute lethal diseases (acute hepatic failure against massive hepatic necrosis, hemorrhagic syndrome) registered in outbreaks of E11 and E19-virus infection in children in the USA, Great Britain, Israel, Russia and Ukraine. Monkeys can be used as man-adequate model for study of enterovirus superacute lethal necrosis of the liver.

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The outbreak of hepatitis E among humans in July-October 1989 in the village of Dzhigdele (140 km to the northeast of Osh) is described. During this outbreak 23 rodents of different species (4 Turkestan rats, 15 house mice and 4 wood mice) were caught within a radial distance of 1 km from the village. 5 out of these 23 animals were found to have hepatitis E virus, detected by the method of immuno-electron microscopy, in their blood sera. Under experimental conditions 7 noninbred white mice were inoculated with material obtained from a previously infected Javanese macaque and a hepatitis E patient. The use of immunoelectron microscopy made it possible to reveal the excretion of the virus with feces on days 4 to 19-23 after inoculation and the development of specific seroconversion in all 7 infected animals. On the basis of these data a suggestion was made that rodents probably played a certain role in the process of the spread of viral hepatitis E.

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Soluble antigen HLA-B27 was assayed in blood serum of 30 patients afflicted with ankylosing spondyloarthritis (AS) and 25 healthy subjects having HLA-B27 (B27+) antigen in the phenotype. As compared to B27+ healthy subjects, B27+ patients with AS demonstrated a significantly higher level of soluble HLA-B27 antigen. A substance whose functional activity was found to be identical to that of soluble HLA-B27 antigen in blood serum of B27- patients with AS was discovered for the first time. It was absent from B27- healthy subjects. In addition to the identification of the fixed forms of soluble HLA-B27 antigen, the assay of this antigen in blood serum enhances the potentialities of laboratory diagnosis of AS, which plays an important role at the early disease stages.

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Serum biochemical parameters were studied in 42 healthy wild-caught adult tamarins (S. mystax), males and females, to determine the normal values. Blood samples were drawn repeatedly, and the serum was tested for aspartate aminotransferase, alanine aminotransferase, isocitric dehydrogenase, serum glucose, serum urea, triglyceride, cholesterol, albumin, and total protein. The results indicated that serum chemistry values were similar to those reported as normal for both humans and other Callitrichidae species. The study of serum biochemical parameters in tamarins with experimental hepatitis A indicated that serum enzyme activities alone reflected the hepatic damage, while other biochemical parameters were of no real clinical importance. The experimental results showed the levels of serum urea to be indicative of the pathological involvement of the kidneys in experimental hepatitis A in some cases.

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A comparative study of hepatitis infection caused by human hepatitis A virus (MS-1 strain), simian hepatitis A virus (AGM-27 strain), and enterically transmitted non-A, non-B hepatitis virus (Tashkent-1435 strain) was carried out. Susceptibility of tamarins to the AGM-27 and Tashkent-1435 as well as to MS-1 strain was demonstrated. All the strains induced an acute infection characterized by serum alanine aminotransferase (ALT) elevation, virus excretion and antibody response. Certain differences in the course of infection caused by these strains were observed in the duration of the incubation period and ALT profiles.

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An experimental batch of inactivated hepatitis A vaccine was prepared using hepatitis A virus (HAV), HAS-15 strain, adapted to cell culture and purified by ultracentrifugation. The vaccine was tested in tamarins immunized intramuscularly three times one month apart. Three tamarins received a vaccine preparation containing 10 ng of immunogen each, three--100 ng each, and three animals were used as controls. The efficacy was judged by the anti-HAV antibody response in the vaccinated animals and development of immunity to subsequent virus challenge two months after the last immunization. The criteria of infection were: elevation of serum alanine aminotransferase, fecal excretion of HAV and production of specific antibody of IgM class. The immune response to 10 ng of the immunogen was lower than to 100 ng, however, both doses produced complete resistance to infection. The booster effect was observed in animals receiving 10 ng of the immunogen. The vaccine batch under study in the indicated doses was shown to have a good immunogenic potency and protective activity for tamarins.

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The development of spontaneous outbreak of hepatitis A (HA) among African green monkeys kept under strict isolation conditions was studied. It was shown that in the case of introduction of HAV the infection involved all the susceptible monkeys, running a course with and without any increase in the level of activity of serum alanine aminotransferase (ALT) After inoculation of commercial gamma-globulin only the infection without the ALT activity increase developed and some monkeys had no signs of HA at all. Experimental reinfection with HAV was produced in monkeys having anti-HAV titres of less than or equal to 1:3500.

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The results of infection of Macaca rhesus monkeys with hepatitis A virus (HAV) strains isolated from monkeys and man are presented. After inoculation of monkeys with human NAV strains the infection could not be reproduced whereas simian HAV strains were found to be pathogenic for M. rhesus monkeys both on experimental inoculation and during natural contacts with infected monkeys in the animal house.

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The results of observations on the pattern of spread of hepatitis A virus and immune response to it in African green monkeys (Cercopithecus aethiops) kept in the animal house are presented. The infection in the monkeys was found to be characterized by all virological, serological, and biochemical parameters inherent in hepatitis A virus. The results indicated that hepatitis A in monkeys may run both asymptomatic and clinically manifest course, and the spread of infection in the animal house sequentially involves most seronegative animals into the epidemic process.

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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.

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The time course of immunopathological symptoms of lupus erythematosus was studied in 117 patients over a period of 5 years. It was established that routine multimodality therapy while resulting in a positive time course of clinical and clinico-biochemical indices, did not ensure the normalization of immunological parameters, particularly of the T-system of immunity. Courses of theophylline and splenin therapy were added to multimodality therapy to raise therapeutic efficacy and to return to normal the status of the immune system. A regular follow-up made it possible to stabilize the disease in 82.1% of the LE patients and to preserve working capacity in 50.4% of them.

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In experiments on parabiotic rats with crossed circulation and separate innervation mechanical or burn trauma of one of the partners was followed by shock-like condition of the other one, and by microcirculatory changes in the mesentery typical of burn or traumatic shock. It shows that in burn shock, as well as in traumatic one, the detected changes in microcirculation are due to humoral, but not to neural factors.

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A long-term training of rats to high-altitude hypoxia (in an altitude chamber at the height of 6500 m, 6 hours daily, for 30 to 40 days) results in a significant hyperemia of their intestinal wall and mesentery. The number of functioning capillaries of trained rats exceeded that of control animals several times, but the blood flow was slowed down in the dilated vessels and their structure was altered. Besides an obvious increase in blood rachemia in the arteries and veins, its rarefaction is observed in the capillaries. Definite hemorheological changes, probably associated with polycythemia, and an increased hematocrite index were noted.

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