Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congenitally athymic nude (Nu/Nu) mice inoculated intraperitoneally with murine cytomegalovirus (MCMV), in doses as low as 1.3 X 10(1) plaque-forming units succumbed to the infection. In contrast, the mean lethal dose for heteroxygous euthymic (Nu/+) littermates was 4 X 10(3) plaque-forming units. Though histopathological changes consistent with MCMV infection were found in the spleen, lungs, and adrenals of nude mice, there were only small focal areas of involvement in the liver. In contrast, Nu/+ mice dying from infection had pathological evidence of severe hepatitis. Spleen cells from immune and control BALB/c mice were injected intravenously into syngeneic mice that had been inoculated previously with lethal doses of MCMV intraperitoneally. Mice receiving 1 X 10(7) or more immune spleen cells were protected against the infection, whereas mice receiving 1 X 10(8) control spleen cells or immune serum were not. Treatment of immune spleen cells with anti-theta serum and complement significantly reduced their protective effect. Immune mechanisms associated with T lymphocytes appear to be critical for recovery from MCMV infection.
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PMID:Role of T lymphocytes in recovery from murine cytomegalovirus infection. 19 22

Up to 3 weeks of age, mice of the resistant A/J strain are fully susceptible to mouse hepatitis virus type 3 infection (MHV3). Immune deficiency, however, resulting from neonatal thymectomy or long term ALS administration led A/J animals to remain susceptible when tested at adult age. Whole spleen cells transferred from normal adult A/J donor mice protected suckling syngeneic recipients from i.p. infection with MHV3. Such a protective capacity of spleen cells was abolished after treatment with anti-theta serum and complement. Spleen cell separation by means of adherence to plastic also showed that neither the nonadherent nor the adherent populations injected separately were able to confer resistance to young mice challenged with the virus. Protection was not achieved with peritoneal cells originating from adult syngeneic animals. Transfer of resistance to MHV3 was obtained, however, when peritoneal cells were associated with adherent spleen cells. This study indicated that two types of mature cells, at least, were required for transferring MHV3 resistance into newborn mice of the A/J strain: T lymphocytes and an adherent spleen cell population.
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PMID:Neonatal susceptibility to MHV3 infection in mice. I. Transfer of resistance. 30 Apr 3

Oral and/or intranasal inoculation of susceptible mouse genotypes with the JHM strain of mouse hepatitis virus (MHV-JHM) consistently results in T cell dysfunction as reflected by in vitro proliferative responses to mitogens or allogeneic cells. One approach to examining the mechanism responsible for the observed functional T cell suppression is to determine whether virus replication is required for its induction. To this end, mice were inoculated oronasally with MHV-JHM that was inactivated with short-wave ultraviolet light, beta-propiolactone or psoralen. Mice were also inoculated with live MHV-JHM after recovery from homotypic or heterotypic MHV infection. Spleen cells from BALB mice inoculated oronasally with inactivated MHV-JHM yielded extremely variable in vitro proliferative responses after concanavalin A stimulation. MHV-susceptible mice exposed oronasally or intraperitoneally to virus inactivated by any of the minimum effective treatments failed to seroconvert. Immunization with psoralen-treated virus intraperitoneally in Freund's complete adjuvant or oronasally failed to protect from live virus challenge, but survivors had elevated virus-specific serum IgG antibody titers compared to mock-immunized controls at two weeks post-challenge. Spleen cells from mice that were challenged after recovery from homotypic live virus infection did not exhibit the profound in vitro T cell suppression normally observed during the acute stage of primary infection. In contrast, MHV-JHM challenge of mice vaccinated with heterotypic live MHV-S resulted in significantly depressed in vitro T cell function. The combined data suggest that either virus replication or exposure to more concentrated antigen may be required for induction of the dramatic T cell dysfunction that occurs as a consequence of MHV-JHM infection as well as for a detectable MHV-specific humoral response.
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PMID:Responses of mice to murine coronavirus immunization. 132 58

Mortality rates among BALB/cByJ, A/JCr, C3H/HeSnJ, and C57BL/6NCr mice inoculated oronasally with mouse hepatitis virus (MHV) strain JHM, ranged from 25 to 67%. Spleen cells harvested from the first three genotypes at 5 days postinoculation proliferated poorly in response to concanavalin A stimulation and produced significantly less interleukin (IL) 2 than cells from uninfected control mice. The function of spleen cells harvested at 14 days postinoculation varied and was host genotype-dependent. Despite clinical signs among some infected C57BL/6NCr mice, spleen cell function was relatively unaffected. C57BL/10ScNCr, B10.A, and SJL/JCr mice remained clinically normal after MHV inoculation. Proliferation and IL2 production by cells from inoculated C57BL/10ScNCr and B10.A mice were similar to responses of their respective controls. In contrast, cells from inoculated SJL/JCr mice were hyper-responsive and produced peak levels of IL2 earlier than control cells. Among the seven genotypes tested, only BALB/cByJ and C3H/HeSnJ spleen cells produced detectable IL4 after primary stimulation with concanavalin A or after priming and restimulation. Primary IL4 production by cells from these two genotypes was significantly reduced if donors were inoculated with MHV 5 days prior to spleen harvest. IL4 production by cells from acutely infected BALB/cByJ mice was considerably enhanced by priming and restimulation.
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PMID:In vitro splenic T cell responses of diverse mouse genotypes after oronasal exposure to mouse hepatitis virus, strain JHM. 165 36

Plasma of cAMP and cGMP in 30 cases of chronic active hepatitis (group of cholestatic patients) as well as in 20 cases of chronic hepatitis with submassive or massive necrosis (group of chronic severe hepatitis patients) were studied with 125I-marked radioimmunoassay. 50 cases with their serum bilirubin levels higher than 171 mumol/L were selected as subjects for this study. Among them, 42 were diagnosed as hepatitis B, 6 as coinfection of hepatitis A and B. According to differentiation of symptoms and signs of TCM, 24 were diagnosed as simple hepatitis due to blood stasis and blood heat, 17 as hepatitis due to blood stasis and blood heat accompanying symptoms of Yang deficiency of the Spleen and Kidney. 20 healthy persons were selected as controls. The results were as follows: cAMP was 56.82 +/- 25.54 ng/L and 80.32 +/- 20.73 ng/L, and cGMP was 9.07 +/- 6.56 ng/L and 19.49 +/- 9.34 ng/L in the group of cholestatic patients and in the group of chronic severe hepatitis patients respectively. Both were higher than those in the control group whose cAMP was 14.12 +/- 3.25 ng/L and cGMP was 5.87 +/- 1.44 ng/L (P less than 0.01). Increase in cGMP and decrease in the ratio of cAMP and cGMP in the cases accompanying symptoms of Yang deficiency of the Spleen and Kidney were much higher than those in the other two types of hepatitis patients (P less than 0.01 and 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relation of changes in plasma cAMP, cGMP and the clinical conditions, pathology and the type of traditional Chinese medicine in 50 cases of chronic severe icteric hepatitis]. 216 73

In contrast to adult mice, young A/J mice, developed an acute hepatitis following infection with Mouse Hepatitis virus type 3. 100% of the young animals died 4 to 5 days after the infection and high levels of virus were found in the liver and peritoneal exudate. Very low levels of IFN-gamma were found in the serum and peritoneal exudate of infected young mice. This was in contrast to the levels observed in adult mice. Spleen cells and macrophage cultures from young A/J mice, again in contrast to adult A/J mice, were shown to be unable to synthesize IFN-gamma and IFN-alpha/beta respectively. Macrophages from either young or adult A/J mice were able to be activated with exogenous recombinant IFN-gamma or IFN-alpha/beta, enabling both sets of cells to restrict MHV3 replication. The results indicate that the ability of the immune system to synthesize IFN-gamma and IFN-alpha/beta may play a major role in the age-dependent resistance of A/J mice to MHV3.
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PMID:A major role of macrophage activation by interferon-gamma during mouse hepatitis virus type 3 infection. II. Age-dependent resistance. 217 34

A total of 102 children aged 5 to 14 years with virus hepatitis B were examined for the status of the mononuclear phagocytic system in accordance with the absolute monocyte count in the circulating blood, esterase and acid phosphatase activity in the monocytes, for function of organ macrophages of the liver and spleen using dynamic scintigraphy with TC-colloid and for macrophages of the skin by the "skin window" method. The rise of the absolute count and lowering of the functional and metabolic activity of blood monocytes were directly proportional to the gravity of virus hepatitis B. The changes persisted for a long time, namely up to 1.5 to 3 months since the disease onset. There was a progressive drop of the functional activity of Kupffer cells in the liver with a maximum decrease seen within 4 to 6 weeks since the disease onset, followed by returning to normal in cyclic disease and preservation of the changes in lingering and chronic virus hepatitis B. Spleen macrophages play an active compensatory role, maintaining normal "purifying" function of the mononuclear phagocytic system. That compensatory response tension appeared high in lingering and especially in chronic virus hepatitis and may serve as a criterion for process chronicity. The changes in the mononuclear phagocytic system observed in cyclic course of mild and medium-gravity virus hepatitis B may be regarded as normal adaptive reaction and do not require any drug correction. The latter one may only be indicated in patients with grave, lingering or chronic disease patterns associated with break down or depletion of the adaptive mechanisms of the system in question.
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PMID:[Functional-metabolic activity of the mononuclear phagocyte system of the blood, liver, spleen and skin in children with hepatitis B]. 225 75

Adoptive transfer of spleen cells from mice 4 days after infection with herpes simplex virus type 2 (HSV-2) reduced the virus titer in the liver of recipient mice infected 24 h before transfer. Macrophage chemotactic factor (CF) and macrophage migration inhibition factor (MIF) were produced by day 3 of infection in spleen cell cultures stimulated with HSV-2, but not with control antigen, i.e. 1 day before the cells are active in adoptive transfer. Interferon was produced in cultures established throughout the infection but not in normal spleen cells. From days 1 to 5 of infection interferon was produced irrespective of in vitro restimulation, although the highest amounts were always produced after stimulation with the specific antigen. Spleen cells from mice infected for 6 days produced interferon only when stimulated with HSV-2. The cells from 6-day-immune mice active in adoptive transfer and CF and MIF production were found to be Thy 1+, Ig- and Lyt2-. Both Thy 1+ and plastic adherent cells were necessary for interferon production, whereas Ig+ and Lyt2+ cells did not produce interferon. The interferon was acid stable and neutralized by antiserum against alpha/beta-interferon and thus has the characteristics of alpha-interferon. The data indicate that a delayed type hypersensitivity reaction with lymphokine-induced macrophage recruitment into infectious foci may be a central feature of the recovery process in HSV-2-induced hepatitis. A possible role of interferon produced by the accumulated cells needs further investigation.
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PMID:Production of lymphokines and interferon by immune cells involved in recovery of mice from herpes simplex virus type 2 hepatitis. 240 97

Mouse hepatitis virus and Sendai virus are among the most common viruses naturally infecting laboratory mice. Concanavalin A-stimulated in vitro proliferative responses of splenocytes were examined after infection of BALB/cByJ mice with the JHM strain of mouse hepatitis virus (MHV-JHM) or Sendai virus. Mice were exposed to these viruses by presumed natural routes (per os or intranasally). Immunodepression was marked but transient among BALB/cByJ mice exposed to MHV-JHM. Among mice exposed to Sendai virus and examined over a 21-day period, spleen cells from only one mouse, sacrificed 10 days postinoculation, exhibited a severely impaired ability to respond to concanavalin A. Lymphokine production by spleen cells from control and infected mice was then assessed. IL 2 was either absent or present at very low levels in culture supernates of concanavalin A-unresponsive spleen cells from MHV-JHM-infected mice. Spleen cells from the single Sendai virus-infected mouse also produced very low levels of IL 2. In contrast, IL 1 was detected in supernatants of all spleen cell cultures derived from control, MHV-JHM-infected, or Sendai virus-infected mice. There was not a clear correlation between concanavalin A responsiveness and the ability of spleen cells to produce interferon-gamma. These results stress the importance of using laboratory mice of known microbiological status for immunologic experiments.
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PMID:Altered splenic T cell function of BALB/cByJ mice infected with mouse hepatitis virus or Sendai virus. 243 94

1. Since the development of resistance against mouse hepatitis virus (JHMV strain) coincides with the maturation of the immune system, we studied the possible role of distinct immunological components in the resistance of adult mice during JHMV infection. 2. Adult C3H mice naturally resistant to JHMV were rendered susceptible to infection by lethal 60Co-irradiation and were subsequently reconstituted with limiting numbers of syngeneic bone marrow cells or spleen cells. 3. Resistance or susceptibility depended on the number of cells used for reconstitution and the interval between reconstitution and infection. Spleen cells from suckling mice affected neither resistance nor susceptibility and peritoneal cells from adult mice and thymus cells reduced resistance. Persistence of JHMV was demonstrated by virus reactivation. 4. Animals infected with JHMV only once before being rendered immunoincompetent showed a different pattern of resistance. One to four months after infection, 15 to 35% of the animals died after reconstitution without having been reinfected, and persisting JHMV was found in their liver, spleen and peritoneal exudate. The survivors (47 to 87%) were resistant to further JHMV infection during immunodeficiency. 5. Animals immunized 3 times with JHMV before irradiation did not show virus reactivation and were fully resistant to JHMV reinfection after reconstitution. The level of neutralizing anti-JHMV serum antibodies in the group of mice immunized only once was comparable with the level of those immunized 3 times. 6. The role of macrophage activation and cell-mediated immunity in this model are discussed as an explanation for the resistance to, and persistence of, JHMV.
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PMID:An immunological analysis of natural resistance to mouse hepatitis virus (JHMV strain) infection in C3H mice. 282 92


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