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Z V Shevtsova

Publications and source records attributed to Z V Shevtsova.

At least 37 records · Page 2Linked to original sources
PubMedDate not supplied

[Virus persistence in hepatitis A in monkeys].

A long-term complex observation of 16 cynomolgus monkeys (Macaca fascicularis) and 8 African green monkeys (Cercopithecus aethiops) with spontaneous and experimental hepatitis A revealed two forms of the illness: acute and chronic. Some monkeys developed undulating chronic course of the disease consisting of 2-6 waves. Others developed relapses (1 to 3) which occurred within 2-4 or 6-11.5 months of the infection. The morphological changes in the liver persisted for 7-28 months. Alaninaminotransferase elevations in the blood and HAV shedding in feces were observed periodically for 7-20 months. HAV persistence was documented by radioimmunoassay, enzyme immunoassay, immune electron microscopy and molecular hybridization. Persisting HAV was shown to remain pathogenic for monkeys. Virological evidence of the etiological association of HAV with chronic infection and late relapses has been obtained for the first time.

Alanine Transaminase↗
PubMedDate not supplied

[Spontaneous and experimental hepatitis A in Papio hamadryas].

Data on high susceptibility of Papio hamadryas to HAV are presented. For the first time, P. hamadryas were shown to be able to respond to both natural and experimental infection developing the features typical of hepatitis A: increased aminotransferase activity, virus shedding in feces, production of anti-HAV IgG and IgM, histological liver lesions. An infection lingering for 3-4 months was observed, as well as a case of chronic experimental hepatitis A with relapse in 7 months of the disease. Virological evidence of HAV infection was obtained in both lingering and chronic disease. HAV-PH strain was isolated for the first time and is described at length. It was isolated from a baboon with spontaneous infection which did not differ from that in man by antigenic and morphological features. The virus replicated in continuous African green monkey kidney cell line (AGMK) and was pathogenic for P. hamadryas. The HAV-PH isolate can be used for modelling hepatitis A in P. hamadryas.

Animals↗
PubMedDate not supplied

[The modelling of hepatitis A in macaques].

Characteristics of experimental hepatitis A in Macaca fascicularis and M. mulatta produced with HAV, strain MP, isolated from M. mulatta in an outbreak of spontaneous hepatitis are presented. The HAV-MP strain induced the disease in all the animals used in the experiment. The infection was manifest, with all virological, serological, biochemical and morphological features typical of hepatitis A. In M. mulatta, the process was protracted, with virus persistence in feces for at least 4 months. Modeling of hepatitis A in Macaca monkeys using HAV-MP strain may be used for the study of the pathogenesis and trials of immune preparations.

Alanine Transaminase↗
PubMedDate not supplied

[The sensitivity of rhesus and cynomolgus macaques to the human hepatitis A virus].

Hepatitis A infection characterized by virus excretion in feces, synthesis of specific IgM antibody, increased activity of alanine aminotransferase in the blood serum, and a complex of morphological lesions in the liver typical of acute hepatitis was reproduced in M. fascicularis (M. f.) and Macaca rhesus (M. r.) using 2 strains of hepatitis A virus (HAV) isolated from human patients. The incubation period varying from 9 to 23 (mean 16) days in M. f. and from 12 to 35 (mean 18) days in M. r. in primary infection shortened to 1-12 (mean 10) and 3-6 (mean 5) days in the process of virus passage from monkey to monkey. The disease was observed to run both manifest forms (except jaundice) typical of human HA and an inapparent form in which the level of enzymes remained within normal limits but HAV could be detected in feces, anti-HAV-IgM in the blood serum, and morphologically acute hepatitis in the liver. Immune electron microscopy of both the initial material and in monkey feces at the levels of all three passages revealed complexes consisting of spherical viral particles 27-29 nm in size coated with antibodies. The immune complexes formed upon addition to the fecal extracts under study of IgG isolated both from human convalescent sera and from sera of experimentally infected monkeys collected in the acute stage of the illness.

Alanine Transaminase↗
PubMedDate not supplied

[Spontaneous hepatitis A with a fatal outcome in rhesus monkeys].

This is the first report of virologically verified spontaneous hepatitis A in M. rhesus monkeys with severe involvement of the liver leading to the death of the animals. In 21 out of 23 dead monkeys morphological lesions in the liver have been characterized as acute hepatitis. In 6 (26%) animals no other pathological processes were found. In 15 animals hepatitis was combined with other diseases (dysentery, parasitic infestations, coronavirus infection). Antigen of hepatitis A virus was detected by an enzyme immunoassay in the intestinal contents of 8 monkeys and in the livers of 3 of them. Immune electron microscopic studies detected in the intestines some virus particles morphologically and antigenically similar to human hepatitis A virus.

Animals↗
PubMedDate not supplied

[The immune structure and specific laboratory indices of acute hepatitis A in lower monkeys of the Sukhumi Nursery].

The study of the rate of occurrence of hepatitis A (HA) markers among monkeys, both newly arriving and those born and living for long periods (aboriginals) in the Sukhumi farm, was carried out. The rate of detection of antibody to HAV (anti-HAV) was shown to vary from 47% (Papio hamadryas) to 100% (Macaca arctoides and Macaca fascicularis). The level of infection with HAV varied among different groups of the same species: Macaca rhesus from 30% to 96%, Papio hamadryas from 0 to 82%. During a long-term observation period seroconversion to HAV was observed in monkeys arriving to the farm from natural habitats. In M. rhesus upon arrival the anti-HAV were detected in 7% and by the end of the observation period reached 100%, in green monkeys 28% and 92%, respectively. Anti-HAV of the IgM class were detected in animals with seroconversion. In fecal extracts from M. rhesus and in the liver, feces, and intestinal contents of green monkeys HAV was found cross-reacting with simian and human sera containing anti-HAV. The virions isolated from a green monkey liver had a buoyant density in CsCl 1.36 g/cm3, and HAV from feces of a M. rhesus sedimented in the density zone of 1.34 g/cm3.

Acute Disease↗
PubMedDate not supplied

[Morphology of coronaviruses from different species of monkeys in the Sukhumi nursery].

The ultrastructure of coronaviruses from 46 out of 111 monkeys examined (baboons, macaques, green monkeys, langurs) was studied by negative staining in homogenates of different parts of the intestinal tract, pancreatic gland, liver, kidneys, lungs, heart, and brain. Because of marked pleomorphism of coronaviruses it is suggested that morphological variants of the viruses may be distinguished. No relationship between pleomorphism of virus particles and species differences of monkeys and their organ pathology was established. Morphological signs distinguishing simian coronaviruses from those of man were noted.

Animals↗
PubMedDate not supplied

[Characteristics of encephalomyocarditis virus isolated from sick monkeys].

A cytopathic filterable agent designated EMC-70 was isolated in 1970 from Macaca rhesus monkeys with encephalomyocarditis. Its biologic and physico-chemical properties were studied. A number of primary and continuous cell cultures were found to be susceptible to the virus, and it was pathogenic for monkeys and small laboratory animals but did not multiply in chick embryos. The virus was stable to chlorofrom, thermolabile, stable to acids, and agglutinated group O erythrocytes of man, sheep, guinea pig. Electron microscopic examinations of infected cells revealed crystalline packings of subunits about 50 nm in diameter typical of picornaviruses. Serological studies demonstrated close antigenic relationship of the isolate with the virus belonging to encephalomyocarditis group.

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