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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Humoral and cell-mediated immune responses were studied in resistant and susceptible strains of mice infected with mouse hepatitis virus type III (MHV 3). Virus was maintained by regular passages in susceptible DBA/2 mice and assayed in DBA/2 mice by LD-50 determination. Normal resistant A strain mice were able to clear the virus from liver, brain, and serum within 7 days after infection. No neutralizing antibody was found. Transfer of serum from immunized A strain mice was not effective in protecting susceptible DBA/2 mice against challenge with virus. In A strain animals resistance to MHV-3 developed rapidly during the 3rd week of life. During the period of susceptibility, newborns were protected neither by transplacental passages of anti-MHV-3 antibodies nor by injection of "educated" thymus cells.
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PMID:Immunopathology of mouse hepatitis virus type 3 infection. Role of humoral and cell-mediated immunity in resistance mechanisms. 16 77

Some biological conditions of the focal necrotic hepatitis test for the differentiation between herpes simplex virus (HSV) types 1 and 2 were investigated. Most of 13 different strains of mice tested were found usable in the test. An upper age limit (4 weeks) for the appearance of focal necrotic liver lesions was found in one strain of mice, while this was not seen in another strain. The minimum dose in 3- to 4-week-old mice was found to be as small as 10(2) to 10(3) p.f.u. in 0.1 ml of diluent. Suckling rats and hamsters, aged up to 7 and 14 days, respectively, were found to be convenient as alternative test animals. Finally, it was observed that focal necrotic hepatitis did not develop in the nude mouse with thymic aplasia on intraperitoneal inoculation of HSV type 2. The possible involvement of the thymus in the pathogenesis of the focal necrotic lesions is briefly discussed.
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PMID:Biological conditions influencing the focal necrotic hepatitis test for differentiation between herpes simplex virus types 1 and 2. 18 7

Type-8 avian adenoviruses were isolated from chickens in a commerical flock suffering an outbreak of inclusion body hepatitis. Serum-neutralizing titer to this type, but not to 7 other types of avian adenovirus, was more than 4 times as high in convalescing chickens as in chickens from the flock bled 2 weeks previously, during the disease outbreak. A disease similar to that in the commercial flock and to inclusion body hepatitis as described in the literature was produced by intra-abdominal inoculation of a type-8 isolant, AMG 5 (2a), into 1-day-old specific-pathogen-free chicks. Pathologic features of the disease included necrotizing hepatitis, pancreatitis, and severe lymphoid depletion of the bursa of Fabricius, thymus, and spleen. It was concluded that type-8 avian adenoviruses were involved in the etiology of the naturally occurring outbreak of inclusion body hepatitis.
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PMID:Involvement of a type-8 avian adenovirus in the etiology of inclusion body hepatitis. 19 Sep 94

Congenitally athymic nude (nu/nu) mice of a BALB/c genetic background were found considerably more resistant to the induction of focal necrotic hepatitis by herpes simplex virus type 2 (HSV-2) tha, were phenotypically normal littermates (nu/+) or BALB/c mice. The augmented resistance was age dependent, as it was only manifested in mice from 4 to 5 weeks of age. Studies of the course of infection showed that nude mice were able to restrain virus multiplication in the liver far better than normal mice in the early phase of infection. However, they seemed inferior to normal mice in eliminating the infectious process. In vitro investigation of peritoneal macrophages revealed that macrophages from 6-week-old nude mice exhibited accelerated spreading and were three times as restrictive in the replication of HSV-2 as macrophages from normal mice. However, no difference was found in the efficiency of adsorption/phagocytosis between macrophages from nude and normal mice. The increased resistance of nude mice could be abolished by blockade of the microphage function of the mice by silica. Nude mice reconstituted at birth with thymus cells were just as susceptible to infection as normal mice. These data suggest that the increased resistance of nude mice to HSV-2 hepatitis is due to the presence of nonspecifically activated macrophages before infection.
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PMID:Role of activated macrophages in resistance of congenitally athymic nude mice to hepatitis induced by herpes simplex virus type 2. 20 7

Twenty 1-day-old specific-pathogen-free chickens each were given an intraabdominal inoculation of either a type-8 avian adenovirus, [AMG 5 (2a], or a type-5 avian adenovirus, inclusion body hepatitis virus (IBHV). The diseases produced were similar. High (60-100%) mortality and statistically significant depression of body weights occurred in both infections. There were necrotizing hepatitis and pancreatitis, lymphoid depletion in the spleen, bursa of Fabricius and thymus, hydropericardium, nephritis and enteritis. Intranuclear inclusions occurred in affected organs. Fluorescent-antibody staining, the Feulgen reaction for deoxyribonucleic acid and electron microscopic studies, as well as studies from the literature, indicated that basophilic inclusions consisted of assembled adenovirions.
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PMID:Comparative study of experimental inclusion body hepatitis of chickens caused by two serotypes of avian adenovirus. 20 21

After intraperitoneal inculation with a virulent mouse hepatitis virus, MHV-3, 50% lethal dose in DDD mice was about 7 log10 higher than that in C3H mice. Histopathologically, splenic lymphocytes especially of the thymus-dependent area were more severely affected in susceptible C3H mice than in DDD mice. In the liver of C3H mice, virus multiplied exponentially after inoculation, attaining 10(6) PFU at moribund stage, while virus multiplication in DDD mice was much less prominent decreasing remarkably at day 5 or later. The virus could multiply in the primary culture of spleen cells from C3H mice but not in those from DDD mice, and cells supporting virus growth seemed to be a theta-positive population of lymphocytes. No difference was observed between the two strains of mice in the ability of peritoneal macrophages to support virus growth in vitro as well as serum interferon levels after infection.
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PMID:T lymphocyte-dependent difference in susceptibility between DDD and C3H mice to mouse hepatitis virus, MHV-3. 23 96

Experiments on mice CBA X C57BL showed that the mixture of cells of the bone marrow, thymus, and spleen from donors with experimental hepatitis caused by carbon tetrachloride and from donors with resection of the normal liver, injected to healthy animals, caused dystrophic changes in the liver; this testifies to the presence of a special clone of cells with a damaging hepatotrophic effect, and participating in the mechanism of autoimmune disturbances in diseases of the liver.
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PMID:[Role of lymphoid cells of the immune system in the genesis of kidney diseases]. 35 Mar 2

In tests on CBAXC57BL mice with experimental hepatitis, induced by carbon tetrachloride, the transplantation of cells from the lymphoid organs of healthy donors intensified the repairing process in the recipient pathologically changed liver. The most pronounced normalization was seen in the liver of the animals given thymocytes which suggests a deficit of these cells in experimental toxic hepatitis and indicates a definite role of the thymus in the repairing processes of the damaged liver.
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PMID:[Effect of transplantation of thymus, bone marrow and spleen cells on the regenerative processes in pathologically changed liver]. 49 89

Aspergillus candidus Link, one of the commonest constituents of cereal mycoflora, produces two kinds of mycotoxins, terphenyllin and xanthoascin, which show different chemical and toxicological properties. The latter, xanthoascin, caused severe hepatic injury with jaundice and focal or confluent necrosis of hepatocytes, when given to mice in doses of 6 mg/kg b.w. or higher by a single subcutaneous injection. With higher doses above 15 mg/kg, myocardial degeneration and necrosis was induced after a week or two in addition to the hepatic injury. Vacuolation of the nuclei of the alveolar interstitial cells of the lung and myocardial interstitial cells was another characteristic lesion caused by this mycotoxin. Other organs including the testicles and thymus were widely involved. The unique nature of lesions in the liver and heart may necessitate further investigations in the field of mycotoxicology in relation to human diseases such as nutritional hepatitis and primary myocardial degeneration.
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PMID:Hepato- and cardiotoxicity of xanthoascin, a new metabolite of A. candidus Link, to mice. I. Blood chemistry and histological changes in mice. 101 75

Peripheral lymphocytes from patients with hepatitis-B surface antigen (HBsAg)-positive and -negative acute hepatitis (AH), chronic active hepatitis (CAH), chronic persistent hepatitis (CPH), and normal controls were tested for in vitro cytotoxicity and blast transformation. Cytotoxicity was measured by chrominum (21Cr) release into the medium from 51Cr-labeled Chang liver cells after incubation for 6 h with peripheral lymphocytes at a lymphocyte target cell ratio of 200:1. Concomitant 72-h incubation studies were performed to assess thymus cell-dependent (T) lymphocyte function as measured by conccanavalin A (Con A)- stimulated incorporation of tritiated thymidine (blast transformation) and by cytotoxicity. It was found that (a) lymphocytes from patients with AH are cytotoxic to Chang liver cells compared to controls (P less than 0.001); (b) lymphocytes from patients with acute and chronic hepatitis are less cytotoxic when incubated with autologous and homologous HB2Ag-positive and -negative AH, CAH, and CPH are as cytotoxic as normal controls when stimulated with a nonspecific mitogen such as Con A; and (d) lymphocytes from patients with CAH while on prednisone therapy showed marked depression of cytotoxicity when stimulated with Con A. Thus these studies show that patients with AH have circulating T lymphocytes which are capable of causing the destruction of Chang liver cells. There is no defect in T-cell function as measured by Con A-stimulated cytotoxicity. There is a serum factor (s) in patients with acute and chronic hepatitis which inhibits spontaneous and induced lymphocyte cytotoxicity and blast transformation. Finally, prednisone treatment appears to inhibit lymphocyte cytotoxicity in patients with CAH.
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PMID:Cell-mediated immunity in acute and chronic hepatitis. 107 30


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