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Macrophages have been described to be important in determining the resistance of A/J mice or the susceptibility of BALB/c mice to the experimental infection with Mouse Hepatitis Virus 3 (MHV3). The interferon gamma (IFN gamma) activation of A/J and BALB/c mouse macrophages was shown to partially restrict the MHV3 replication only in macrophages from the resistant A/J mice. The activation by IFN gamma and/or infection with MHV3 showed that BALB/c mouse macrophages were capable of releasing tumor necrosis factor alpha (TNF alpha), interleukin 1 (IL-1) and anion superoxide (O2-), and A/J mouse macrophages were capable of releasing TNF alpha and IL-1 but not O2-. Comparable amounts of TNF alpha or IL-1 were released by IFN gamma-activated A/J or BALB/c mouse macrophages. Following MHV3 infection or IFN gamma activation and MHV3 infection, BALB/c mouse macrophages were always capable of releasing higher amounts of TNF alpha, IL-1 or O2- than A/J mouse macrophages, which correlated with their susceptibility to the virus infection. The data indicate that the anti-MHV3 effect induced by IFN gamma in A/J mouse macrophages is not related to the studied extrinsic activities of these cells.

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The possible role of interferon-gamma (IFN-gamma) in the resistance of A/J mice to MHV3 infection was investigated. Monoclonal antibodies specific for IFN-gamma, CD4 and CD8 molecules were administered in vivo to deplete selectively the IFN-gamma synthesized or the appropriate subset of T cells. The animals were then infected with MHV3 and the course of infection was followed by studying different parameters, such as, the mortality, the virus growth in the tissues and the IFN-gamma synthesis in sera and peritoneal exudates. After MHV3 infection, a full resistance of control A/J mice was observed, in contrast to the high mortality rate observed among the depleted animals, where higher virus titers were found in different tissues. The IFN-gamma synthesis in sera and peritoneal exudates of depleted mice, after MHV3 infection, drastically decreased when compared to that detected in control mice. The data presented are consistent with the hypothesis that IFN-gamma plays an essential role in the resistance of A/J mice to MHV3 infection.

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A fatal disease of rabbits was first reported in the People's Republic of China in 1984. Since 1986, the disease has been reported in most countries of Europe and in the Republic of Korea. In 1989 a similar disease, presumably linked to the importation of rabbit meat from the People's Republic of China, spread rapidly through ten states in Mexico; it was eradicated during the same year by "stamping-out" measures. In Mexico, as was the case in other outbreaks, morbidity and mortality reached 80-90% with few clinical signs. In pathogenesis studies, the primary sites of replication were in the small intestinal crypt and villous epithelium, hepatocytes and splenic lymphocytes. Many organs, including the lung and kidney, contained acutely infarcted tissue and haemorrhages resulting from a terminal disseminated intravascular coagulopathy. The disease and the characteristics of the virus isolated in Mexico are similar to isolates from Europe and the Republic of Korea. The comparative morphologic, from Europe and the Republic of Korea. The comparative morphologic, immunologic, and in situ nucleic acid hybridization evidence for a parvovirus aetiology are summarized.

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Se elaboraron dos vacunas experimentales (Vac-19 y Vac-28) de Hepatitis a Cuerpo de Inclusión (HCI) a partir de los serotipos 4,10 y 11, aislados en brotes de campo en el país. Las cepas se atenuaron por pasajes en huevos embrionados SPF (16 y 22 pasajes para ambas vacunas) y cultivo de células renales (3 y 6 pasajes respectivamente). Se utilizaron cuatro grupos (G) experimentales: G I y G II formado por 8 pollos cada uno, vacunados vía oral (4,4 DICC55/ml) con Vac-19 y Vac-28 respectivamente a la tercera semana y revacunados a los 35 días por igual vía y dosis. Los grupos G III y G IV con 5 pollos cada uno correspondieron a control positivo y negativo, ambos grupos sin vacunar, el primero solo desafiado con un pool de los serotipos 4,10 y 11, a los 45 días de edad y el último sin desafiar. Exámenes clínicos serológicos se realizaron previo y posterior a las vacunaciones y desafío. La respuesta inmune se midió, a través de Inmunodifusión en Gelosa (IDG) y Seroneutralización (SN) en Cultivo de Células Renales (CCR) por el método ß (200 DICC50/50*l). Mediante la prueba IDG se observaron reacciones positivas (100%) desde el día 43 en adelante en los grupos cavunados y desde el 55 en el grupo desafiado (GIII). Los Títulos Medios Geométricos (TMG) previo al desafío fueron G I de 1.194 y en G II 23.525. Con posterioridad al desafío se observó un TMG de 7.760 y . 305.736 respectivamente en ambos grupos. El G III tuvo un TMG de 640. No se observó signología clínica y mortalidad el desarrollo de la experiencia. Se concluye que solo Vac-28 originó protección a las aves, emdida por la respuesta inmune humoral, pero por las lesiones observadas en el grupo solo vacunado se debería continuar estudiando sucompleta atenuación

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Infectious Canine Hepatitis virus was isolated from 10 of 51 tested dogs caught in São Paulo and neighbouring Districts. The viruses were isolated in dog kidney cell cultures from fecal specimens and, in two instances, from the non-inoculated cell cultures themselves. All the isolated virus strains presented biological and physicochemical characteristics proper to the adenovirus and were immunologically identified as ICH virus. Specific neutralizing antibodies to the ICH virus were found in 50% of the dogs with negative virus isolations in titers from 1/500 to 1/25,000. These results point to a very high frequency of infection by the ICH virus in the sample studied.

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