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

We investigated LEC rats immunopathologically which spontaneously developed hepatitis to find out the genesis, in comparison with non-hepatitis LEA (Long Evans Agouti) rats. 1) Wet weights of the spleen and thymus of 6-week old LEC rats were significantly lighter than those of LEA rats of the same age. 2) Serum IgG (Immunoglobulin G) in LEC rats remained markedly low after the age of two months and IgG antibody formation to SRBC (Sheep Red Blood Cell) as detected by plaque assay was also significantly suppressed. On the other hand, IgM antibody formation to SRBC was significantly suppressed through serum IgM level in LEC rats was normal or rather increased. 3) Blastogenic responses of spleen cells to PHA and Con A were much more suppressed in LEC rats than in LEA rats. 4) Cytostatic activity of intraperitoneal macrophages against tumor cells was more evident in LEC rats than in LEA rats, but there was no difference in NK (natural killer) activity between the two rat strains. From these results, it is speculated that spontaneously hepatitis-developing LEC rats possess T and B cell deficiency (combined immunodeficiency) and that the increase of macrophage and NK cell activities are linked to the genesis of developing hepatitis.
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PMID:[Combined immunodeficiency in LEC (Long Evans Cinnamon) rats with spontaneous hepatitis]. 279 59

Individual triple plaque purified strains of attenuated duck hepatitis virus can protect ducklings against virulent challenge with the virus but they are as genetically unstable as their parent vaccine strains and are transmissible by direct contact. The use of rapid passage is advocated as a method to improve these parameters.
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PMID:Triple plaque purified strains of duck hepatitis virus and their potential as vaccines. 282 8

It has previously been shown that the murine coronavirus mouse hepatitis virus (MHV) undergoes RNA recombination at a relatively high frequency in both tissue culture and infected animals. Thus far, all of the recombination sites had been localized at the 5' half of the RNA genome. We have now performed a cross between MHV-2, a fusion-negative murine coronavirus, and a temperature-sensitive mutant of the A59 strain of MHV, which is fusion positive at the permissive temperature. By selecting fusion-positive viruses at the nonpermissive temperature, we isolated several recombinants containing multiple crossovers in a single genome. Some of the recombinants became fusion negative during the plaque purification. The fusion ability of the recombinants parallels the presence or absence of the A59 genomic sequences encoding peplomers. Several of the recombinants have crossovers within 3' end genes which encode viral structural proteins, N and E1. These recombination sites were not specifically selected with the selection markers used. This finding, together with results of previous recombination studies, indicates that RNA recombination can occur almost anywhere from the 5' end to the 3' end along the entire genome. The data also show that the replacement of A59 genetic sequences at the 5' end of gene C, which encodes the peplomer protein, with the fusion-negative MHV-2 sequences do not affect the fusion ability of the recombinant viruses. Thus, the crucial determinant for the fusion-inducing capability appears to reside in the more carboxyl portion of the peplomer protein.
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PMID:RNA recombination of murine coronaviruses: recombination between fusion-positive mouse hepatitis virus A59 and fusion-negative mouse hepatitis virus 2. 283 4

Experiments were undertaken to study the pathogenesis of VRI-33, a strain of fowl adenovirus serotype 8 isolated from the liver of a broiler chicken with inclusion body hepatitis. A 30% death rate resulted from oral infection of one-day-old specific pathogen free chickens with 10(6) plaque forming units of VRI-33. Chickens 10, 14, 21 and 28 days of age did not die following infection via natural routes but there were some motalities following infection via parenteral routes. Immunodepression by neonatal cyclophosphamide treatment, followed by infection with VRI-33 via non-parenteral routes, caused varying degrees of hepatitis with basophilic intranuclear inclusion bodies in hepatocytes. The mortality rate of cyclophosphamide-treated, VRI-33 infected chickens, was not significantly altered by post-infection temperature stress. Infection with infectious bursal disease virus, followed by infection with VRI-33 via natural routes at 14 days of age, was not associated with mortalities.
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PMID:Pathogenicity studies with a strain of fowl adenovirus serotype 8 (VRI-33) in chickens. 283 9

A study was undertaken to determine the safety and suitability of vaccinia virus as an eukaryotic expression vector in dogs. Clinical signs were not seen in inoculated dogs, with the exception of small nodules at the site of inoculation. Vaccinia virus did not spread from dogs that were inoculated by SC (n = 5), intradermal (ID; n = 13), or intranasal (n = 3) routes to noninoculated dogs maintained in close contact. Replication of vaccinia virus appeared to be restricted in dogs because greater than or equal to 10(5) plaque-forming units of virus were required to induce an immune response by ID inoculation. Results were better with ID inoculation than with SC or intranasal inoculations. Repeated inoculations enhanced serum antibody titers, and annual reinoculation resulted in boosting of antibody titers. Maternal antibody interfered with virus replication and antibody production. Recombinant virus products induced antibody formation in dogs to human influenza-A virus, herpes simplex virus, and human hepatitis-B virus antigens. It was concluded that vaccinia virus would be safe and suitable as an eukaryotic expression vector in dogs.
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PMID:Immune response to vaccinia virus and recombinant virus products in dogs. 297 18

Since patients with primary biliary cirrhosis (PBC) have evidence of abnormal function of the humoral immune system, we determined if B cells from patients with this disease show evidence of activation and can be stimulated by polyclonal activators. Using a reverse hemolytic plaque assay, it was found that patients with PBC had a significant increase in the number of circulating immunoglobulin-secreting cells, compared to normal controls and patients with chronic type B hepatitis virus (HBV) infection. However, the total number of activated cells was less than 1% of the total circulating B-cell population. Furthermore, we were unable to detect an increase in the expression of transferrin receptors, a membrane receptor associated with B-cell activation, in the majority of B cells in patients with PBC. In other studies, immunoglobulin production by lymphocytes from patients with PBC, when stimulated with the polyclonal activators pokeweed mitogen and Epstein-Barr virus (EBV), was reduced. This hyporesponsiveness was not due to a decrease in the number of B cells, as determined by staining with the monoclonal antibody anti-Leu 12. Furthermore, the decreased response to B cells to polyclonal activation in PBC patients was not due increased suppressor T-cell function, since EBV-simulated cultures of lymphocytes from patients with PBC demonstrated diminished suppression of immunoglobulin-secreting cells after 14 days of culture compared to controls. These findings suggest that the humoral abnormalities in PBC are due to the activation of a small subpopulation of B cells rather than to generalized B-cell hyperactivity.
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PMID:Circulating activated B cells in primary biliary cirrhosis. 299 32

After infection with 10(3) plaque-forming units of mouse hepatitis virus strain 3 (MHV-3) in vivo, peripheral blood mononuclear cells and splenic cells expressed procoagulant activity (PCA) in a pattern directly correlating with susceptibility to disease. Mononuclear cells from BALB/cJ mice, a strain which is fully susceptible to MHV-3, expressed a greater than 500-fold increase in PCA. PCA was first detected within 12 hr of infection; prior to histologic evidence of disease and viral replication, it reached maximal levels 48 hr post-infection (p.i.) and persisted until the death of the animals 5 to 7 days p.i. Mononuclear cells from C3HeB/FeJ mice expressed a significant but lesser titer of PCA, with elevated PCA persisting throughout the chronically infected state until death of the animals 4 to 6 mo p.i. Basal levels of PCA were detected in mononuclear cells from fully resistant A/J mice despite the presence of large amounts of virus in livers, spleens, and sera from these animals. When mononuclear cells expressing high PCA were subfractionated, monocytes were found to be the cellular source of greater than 96% of the PCA activity. Increased plasminogen activator activity was found in monocytes from resistant A/J mice at the time when PCA was markedly elevated in BALB/cJ and C3HeB/FeJ mice. This activity persisted for 5 to 7 days p.i., but was undetectable 10 days p.i. at a time when the mice had cleared the virus from their blood streams. These observations suggest that monocyte PCA may be important in the pathogenesis of MHV-3 disease, whereas the production of monocyte plasminogen activators may contribute to resistance of A/J mice to MHV-3-induced liver disease.
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PMID:The immune response to mouse hepatitis virus: expression of monocyte procoagulant activity and plasminogen activator during infection in vivo. 299 39

An assay to determine 50 per cent neutralisation end points of duck anti-duck hepatitis virus sera was developed using a plaque assay to quantify residual virus. The optimal conditions were determined. Ducklings produce a serological response within four days of vaccination and the response reaches a maximum within nine days.
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PMID:Duck hepatitis virus: adaptation of a plaque assay to determine 50 per cent end points with duck sera. 303 61

The immunoglobulin production capacities of peripheral blood lymphocytes obtained from patients with various chronic inflammatory liver diseases and from normal individuals were compared. Using a reverse hemolytic plaque assay, immunoglobulin-secreting cells (ISC) were counted immediately after isolation (immediate ISC) and again after 6-day, in vitro cultivation without stimulant (spontaneous ISC) or in the presence of pokeweed mitogen, PWM (PWM-induced ISC). An increased number of immediate ISC were observed in patients with chronic active hepatitis (CAH) of the autoimmune type (n = 7) or with CAH type B (n = 32), probably reflecting a defect of the in vivo suppressor cell system as previously demonstrated. In vitro preincubation of cells with 5 x 10(-8) M prednisolone reduced the increase in the number of immediate ISC in patients with CAH of the autoimmune type. On the other hand, lymphocytes obtained from patients with CAH-type NANB (n = 9) and with primary biliary cirrhosis (PBC) (n = 12) showed an impaired capacity to generate ISC upon stimulation with PWM. Spontaneous ISC from patients' lymphocytes were not significantly different from those of normal individuals. Using allogeneic co-cultures with lymphocytes from normal individuals and from patients with CAH NANB hepatitis or primary biliary cirrhosis, we observed no increase in suppressor cell activity. Therefore, the diminished responses to PWM are probably attributable to an alteration in the peripheral helper T-cell compartment.
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PMID:Abnormalities of B cell activation and immunoregulation in patients with chronic inflammatory liver diseases. 306 20

The genomic RNA and intracellular RNA of mouse hepatitis virus, strain JHM (MHV-JHM) and two plaque mutants (1a and 2c), which have been isolated from a persistently infected culture (JHM-CC), have been analyzed by T1-resistant oligonucleotide finger-printing. The genomic RNA of the virus population (JHM-CC virus) released from different passage levels of the same persistent infection has also been analyzed. The analysis shows the locations within the genomic and intracellular RNAs of more than 45 T1-resistant oligonucleotides and confirm earlier studies (J. L. Leibowitz, K. C. Wilhelmsen, and C. W. Bond (1981), Virology 114, 39-51), showing that the six subgenomic RNAs of MHV-JHM form a 3' coterminal nested set which extends for different lengths in a 5' direction. The analysis also identifies in each subgenomic RNA those large T1 oligonucleotides derived from noncontiguous regions of the genome during mRNA synthesis. Two important conclusions can be reached from analysis of the mutant viruses. First, the virus population released from the persistent infection represents a fairly constant mixture of viruses, and the fluctuating emergence of variants as predominant species in the culture does not occur. Second, the data indicate that for particular intracellular RNAs of mutant viruses the sequence rearrangements occurring during subgenomic mRNA synthesis are different from those in the corresponding intracellular RNA of wild-type virus. The result may indicate a potential flexibility in the leader/body fusion process that has not been previously recognized.
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PMID:Analysis of genomic and intracellular viral RNAs of small plaque mutants of mouse hepatitis virus, JHM strain. 609 79


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