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Biomedical subjects

M I Berría

Publications and source records attributed to M I Berría.

At least 37 records · Page 2Linked to original sources
PubMed1989

Astrocytic reaction predominance in chronic encephalitis of Junin virus-infected rats.

Junin virus antigen distribution and astrocytic reaction to prolonged infection were characterized in rat brain by the PAP technique. During the acute stage of neurologic disease following intracerebral inoculation, Junin antigen was detected in 100% of animals, strongly in most neurons but also to a much lesser degree in scattered astrocytes, dropping to 20% of rats at 540 days postinfection. Initially labeled in all brain areas, viral antigen gradually disappeared from hippocampus but persisted irregularly in cerebral cortex, basal ganglia, Purkinje cells, pons, and medulla oblongata. Such a pattern suggests that specific neuronal subpopulations, in spite of apparently unaltered cell morphology, may persistently harbor the virus, leading on occasion to a delayed neurologic syndrome. During both the acute and chronic stages of disease, a mild inflammatory exudate was observed, characterized by the presence of T and B lymphocytes, as well as macrophages and unidentified round cells. GFAP immunostaining showed increased astrocytic reaction as infection lapsed into chronicity. Corpus callosum, hippocampus, and cerebellum exhibited the sharpest reactive astrocytosis, followed by basal ganglia, pons, and medulla oblongata, whereas in cerebral cortex it was considerably less. Astrocyte activation, which failed to correlate with viral antigen presence in neurons, seems to result from a generalized condition, possibly including diffusible brain factors triggered by viral infection. Such widespread astroglial reaction may thus contribute to the outcome of the late neurologic syndrome.

Animals↗
PubMed1986

Chronic neurologic disease in Junín virus-infected rats.

The purpose of this study was to determine whether Junín virus persistence in CNS of rats was capable of inducing late neurologic disease. Following intracerebral inoculation of newborn animals with XJ strain, three distinct stages could be discerned: an early phase of acute disease, up to 30 days pi, with 5% mortality; an intermediate one, extending to 280 days pi, without clinical signs but with evident viral persistence; and a final period of chronic illness, featuring clinical neurologic syndrome, severe perivascular inflammatory reaction, PAP-labeled viral antigen in a few cerebral and cerebellar neurons, and virus recovery only by coculture. Late neurologic disease seems associated to the lack of effective clearance of brain virus, leading to viral persistence and long lasting immunologic stimulation. The importance of animal models for pathogenic studies on CNS persistent viral infections leading to late neurologic disease is stressed.

Animals↗
PubMed1985

Astrocyte differentiation induced by Junín virus in rat brain cell cultures.

Morphological and immunocytochemical differentiation was observed in astroglial cell cultures of the rat infected with Junín virus. From days 3 to 6 postinoculation (p.i.), GFAP immunostaining was observed in both the perikaryon and processes of maturated astrocytes, whereas it was limited to the perikaryon in less differentiated cells. The rather slow spontaneous differentiation usually occurring in astroglial cell cultures was seen to be accelerated by viral infection, mimicking the astrocytic reaction formerly described in Junín virus-inoculated mice. Infected cell monolayers showed orderly development, maintenance of contact inhibition, and exhaustion of cell cultures beyond the 6th-7th passages. The morphological and immunocytochemical maturation effects of Junín virus on astroglial cells were evident, but to a significantly lesser degree than those caused by rat brain extract. The glial cell cultures proved a valuable tool for the study of virus-cell interaction, since the immune response and the structural complexity of the whole animal can thus be avoided.

Animals↗
PubMed1984

Melatonin inhibits beta-adrenoceptor-stimulated cyclic AMP accumulation in rat astroglial cell cultures.

We investigated whether astroglial cells are a site of action for the effect of melatonin on brain cyclic AMP content. Rat astroglial cell subcultures, identified according to morphological and immunochemical criteria, were used. Addition of melatonin to the cultures did not result in changes of cyclic AMP content. However, melatonin at 0.1-1 microM concentrations was able to impair the cyclic AMP increase elicited by 1 microM norepinephrine or isoproterenol in astroglial cultures. This melatonin effect was also shared by its biologically active analogues 5-methoxytryptophol and 6-chloromelatonin. Serotonin was only effective at a 100-fold greater concentration, while the biologically inactive melatonin metabolite 6-hydroxymelatonin was devoid of activity at any concentration used. These results suggest that methoxyindoles modulate negatively beta-adrenoceptor-induced cyclic AMP accumulation in cultured rat astroglial cells.

Animals↗
PubMed1984

Transplacental infection in guinea pigs inoculated with an attenuated strain of Junin virus.

Transplacental infection by the attenuated XJC13 strain of Junin virus (JV) in the guinea pig model was evaluated. 5 pregnant guinea pigs were infected intramuscularly at 45 +/- 3 days of pregnancy. 4 animals were killed at 14 days postinfection (p.i.), and 1 was sacrificed at 137 days p.i. at the end of its second pregnancy. Evidence of JV was obtained by Vero cell cocultivation in all 14 fetuses harvested (brain and/or spleen) and in 10 of 11 placentas. The results strongly suggest that the attenuated JV strain infected the fetus by the transplacental route, as previously demonstrated for the pathogenic XJ strain. Despite limited sampling, the acute as well as the chronic stage proved viable.

Animals↗
PubMed1983

Immunoperoxidase study of astrocytic reaction in Junín virus encephalomyelitis of mice.

Intracerebral inoculation of strain XJ Clon 3 of Junín virus into 1-2-day-old mice resulted in the appearance of viral antigen, detectable by means of the peroxidase antiperoxidase (PAP) technique, within the cytoplasm of the neurons of the cerebral cortex, the basal nuclei, cerebellum, pons, medulla, spinal cord, and spinal ganglia; Junín antigen was likewise observed, although to a lesser extent, in the cytoplasm of astrocytes. The viral antigen was found in highest concentration at the cytoplasmic periphery, near the cell membrane, where complete virions are formed by budding. In some cells a "tigroid" distribution of the antigen was observed, suggestive of its production and concentration within the granular endoplasmic reticulum. In spite of the heavy infection of the neural structures, the neurons did not always show major alterations. By immunolabeling of the glial fibrillary acidic protein (GFAP) by the PAP method, a severe glial response could be seen in infected mice, featuring hyperplasia, hypertrophy, and shape distortion of the astrocytes. This easy labeling was not observed in normal mice of the same age, and suggests the accelerated maturation of the astrocytes and the increased GFAP synthesis by direct action of the virus upon such cells. In view of its specificity, use of the PAP technique for GFAP immunolabeling will most likely replace the traditional metal impregnation methods in the study of the astrocytes. Its utilization would be indicated whenever astroglial changes are suspected in any CNS pathologic condition.

Animals↗
PubMed1974

Ultrastructure of Junín virus in mouse whole brain and mouse brain tissue cultures.

Comparative ultrastructural studies were performed on the development of Junín virus in mouse brain and in cerebellum explants and brain monolayers of the same animal. In mouse brain, neurons and astrocytes released virus particles by a budding mechanism identical to that previously described for this virus. In the neurons, the viral multiplication took place in the perikarion as well as in the cytoplasmic processes, including areas near synapses. Viral particles were observed emerging from pericapillary neurons and astrocytes. In the explants, the budding also occurred in neurons and astrocytes. In the monolayers, however, the virus originated in astrocytes and cells of fibroblastic appearance, which were the two cell types that developed in this substrate. These results indicate that the characteristics of the development of Junín virus in mouse brain are faithfully reproduced in cerebellum explants from the same animal, thus allowing some extrapolation of data from one system to the other. The explant proved to be a better model than the monolayer, not only because it reproduced the structural complexity of nervous tissue better, but also because it contains neurons and astrocytes, i.e., the two cell types that release the virus in the in vivo system.

Animals↗
PubMed1969

Morphogenesis of aura virus.

Aura virus, a member of the Western equine-encephalitis-Whataroa subgroup of group A arboviruses, was studied by electron microscopy in suckling mouse brain and chick embryo cultured cells. Virus precursors, budding particles, and complete virus particles were first detected 10 hr after infection in chick embryo cells and 24 hr after inoculation in mouse brain. Virus precursors were generally seen aligned along cytomembranes, and were less frequently seen closely associated with viroplasm-like foci, tubular aggregates, or scattered in the cytoplasmic matrix without an apparent connection to any other structure. The assembly of mature virus was observed to take place by a budding process of the virus precursor from the plasma membrane into the extracellular space, and from the cytoplasmic membranes into the lumina of vacuoles and cisternae. It was demonstrated that the endoplasmic reticulum participates in the assembly of intracellular virions. Indirect evidence was found to indicate that the Golgi complex may also form mature virus. Aura virions had a size, shape, and structure similar to those of the previously described group A arboviruses.

Journal Article↗
PubMedDate not supplied

Theiler virus-GDVII strain (TMEV-GDVII) infection of cultured astrocytes. An image analysis of its effects on cell activation.

Our original aim was to determine whether dBcAMP-induced activation of cultured astrocytes affected the course of subsequent viral infection. After 2 h exposure of 2-day-old first subculture of mouse astrocytes to dBcAMP 1 mM, cell monolayers grown in glass coverslips of Leighton tubes were inoculated with 10(3) PFU of Theiler virus-GDVII strain (TMEV-GDVII). At 9 days post-infection (pi), viral infectivity persisted in supernatants from dBcAMP-treated cultures, but was no longer detectable in non-stimulated controls. The relatively spared astroglial monolayer at day 1 pi, hardly affected by progressive viral cytolytic effect, was chosen for immunolabeled cell count, whether by viral antigen or GFAP. To this end, 20 fields for each coverslip were digitalized at 250x final magnification. In dBcAMP treated cultures, viral antigen(+) cells were fewer and lower in percentage versus infected cultures lacking stimulation. As regards GFAP staining, stimulation or infection per se induced a greater number and percentage of labeled astrocytes. According to morphometric characterization, such increase was due to a greater number of process-bearing astrocytes. It may be concluded that, regardless of previous dBcAMP treatment, early TMEV-GDVII infection enhanced immunocytochemical and morphological differentiation in cultured astrocytes.

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