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)

One patient with hepatitis-B surface antigen (HBsAg)-positive chronic aggressive hepatitis, and two chimpanzee carriers of HBsAg, were each given seven doses of 10(7) I.U. of human fibroblast interferon over two weeks. The main differnce observed after treatment was a depression of the nucleocapsid hepatitis-0 core antigen in the liver, indicating that hepatitis-B virus infection is sensitive to interferon. Except for a short febrile reaction, no undesirable effects were seen after the administration of human fibroblast interferon which has not been previously given to man.
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PMID:Administration of human fibroblast interferon in chronic hepatitis-B infection. 6 May 13

Chimpanzees chronically infected with hepatitis-B virus showed transient changes in several markers of infection when treated with the interferon inducer polyriboinosinic-polyribocytidylic acid-poly-l-lysine carboxymethyl cellulose. Serum Dane-particle-associated D.N.A. polymerase, e antigen and hepatitis-B surface antigen, and intrahepatic hepatitis-B surface and core antigens diminished during treatment. Defective (D.N.A.-polymerase-negative) Dane particles increased in titre transiently during treatment; these may play a role in the modulation of hepatitis-B virus infection. Humoral immune responses in chronic hepatitis-B carrier chimps were unaffected. Interferon inducers (or exogenous interferon) may be useful for the treatment of chronic hepatitis-B virus infection.
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PMID:Modification of chronic hepatitis-B virus infection in chimpanzees by administration of an interferon inducer. 6 40

In viral hepatitis A, we could distinguish between monophasic and polyphasic forms. Monophasic and polyphasic hepatitis A induce the production of plasma interferon. Interferon level, elevated as early as the first days following the appearance of clinical signs, decreases and reaches a minimum value on the seventh day. A new rise of interferon is characterized by a maximum level on the twelfth day and a minimum level on the thirtieth. Beyond the first month we could still detect the presence of interferon. In the two forms of hepatitis, a complement system is activated both by classical and alternate pathways. IgM levels increase early, IgA levels remain unchanged. On the other hand, IgG levels, only slightly elevated in monophasic hepatitis A, are highly increased in polyphasic hepatitis A beyond the first month. Alpha 2-macroglobulin reaches levels above normal during convalescence in monophasic hepatitis A; on the contrary, in polyphasic hepatitis A, alpha 2-macroglobulin levles are above normal as early as the thirty first days of illness and remain above normal for several months. Elevated levels in alpha 2-macroglobulin may inhibit cellular immunity which is accountable for immunological injury of virus infected hepatocytes. We wonder whether this earlier increase in alpha 2-macroglobulin is responsible for the lasting character of viral infection observed in polyphasic hepatitis A.
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PMID:[Production of interferon and alpha 2-macroglobulin involvement in immune response during human viral hepatitis A (author's transl)]. 6 8

Four-week-old weanling mice survived, whereas 1-week-old suckling mice died, after intraperitoneal inoculation of mouse hepatitis virus, MHV-S strain. The factors involved in this difference in susceptibility were studied. After virus inoculation, differences in virus growth in the liver and spleen were observed, which correlated with the susceptibility of animals to the virus. Interferon, detected at an early stage of infection, was considerably lower in suckling mice than in weanling mice. Titers of MHV-S in peritoneal cells from infected animals were at least 100 times greater in suckling than in weanling mice, and a similar, but less prominent difference in virus growth was also found in the corresponding cultured macrophages. After transfer of peritoneal cells from weanling to suckling mice, a decrease in mortality of infected suckling mice was observed. These results suggest that both interferon and macrophages may be important in the age-dependent resistance of mice to MHV-S infection.
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PMID:Factors involved in the age-dependent resistance of mice infected with low-virulence mouse hepatitis virus. 9 38

Since a decreased interferon response has been linked with certain chronic viral infections, a preliminary study was undertaken to determine whether an altered interferon response may be involved in the pathogenesis of chronic hepatitis, a complication of type B hepatitis. The production of interferon by lymphocytes from patients with chronic hepatitis was compared with the production by lymphocytes from normal subjects. The amount of interferon produced by paramyxovirus-stimulated lymphocytes from 16 patients was substantially smaller than that produced by lymphocytes from 12 healthy donors. The results indicate that decreased production of interferon may be responsible for the chronicity of the disease. However, further studies are necessary to establish causality.
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PMID:Decreased interferon response by lymphocytes from children with chronic hepatitis. 17 16

In supernatants of mixed mouse spleen cell cultures established for 4 days, a species-specific inhibitor of virus replication with a broad antiviral spectrum was found. The inhibitor was destroyed by trypsin, was nondialyzable and acid labile, and was not neutralized by antibody to mouse L cell interferon. This indicates that in mixed lymphocyte cultures a type II interferon is made that has no immunological relationship with "fibroblast" interferon. This leukocyte product was shown to protect mouse hepatitis viruses. It is suggested that lymphocyte interferon may collaborate with macrophages in host defense against viruses, as a mediator of cellular immunity.
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PMID:Production by mixed lymphocyte cultures of a type II interferon able to protect macrophages against virus infection. 19 17

Two assays of cell-mediated immunity, lymphocyte transformation and interferon production, were adapted to test for specific immunity to cytomegalovirus (CMV). Normal individuals seropositive for CMV had a mean transformation index of 7.9 in response to antigen of the Davis strain of CMV, whereas all of 14 seronegative normal individuals had transformation indexes of less than or equal to 3.0. Interferon production in seropositive and seronegative individuals was not statistically different. One to two months after CMV mononucleosis (after the termination of viruria), normal individuals had increased transformation indexes. Recipients of cardiac transplants within six months after transplant had normal levels of antibody to CMV; lymphocyte transformation and interferon production in these subjects were markedly decreased and returned to normal by three years and between one and three years after transplant, respectively. A syndrome of unexplained fever, hepatitis, pneumonitis, leukopenia, and atypical lymphocytes was common in a group of recipients with primary CMV infection. Shedding of virus was frequent in these symptomatic patients and in patients with repeat infection during the first three years after transplant. These assays appear to identify periods of immune deficits correlating with increased incidence of infection with CMV.
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PMID:Cell-mediated immunity of cytomegalovirus infection in normal subjects and cardiac transplant patients. 20 83

All human, simian, bovine and avian adenovirus types tested so far and the canine hepatitis virus induce interferon production in chick cells. This finding indicated this property to be characteristic for viruses belonging to the adenovirus group. Trypsin treatment, which had no effect upon the infectivity, diminished or eliminated the interferon-inducing abilities of crude adenoviruses, and thus the need for a trypsin-sensitive protein in interferon induction was suggested. T antigen and interferon were formed simultaneously in chick embryo fibroblast cells infected with human adenovirus type 12, and therefore the adenovirus-specific T antigen was resistant to the action of endogenous interferon synthetized by the same cells. In chicks inoculated with human types, the appearance of interferon was biphasic: an 'early' and a 'late' interferon could be demonstrated with maximum titre 4 and 10 hr, respectively, after virus infection. In chicks infected with adenoviruses, first interferon production and then a decreased primary immune response to sheep red blood cells was observed. It was assumed that in adenovirus-infected chicks the interferon produced by viral stimulus resulted in a transient immunosuppression.
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PMID:Interferon induction by adenoviruses. 22 39

Nude mice which had received intraperitoneal injection of silica simultaneously with infection of mouse hepatitis virus, NuU strain, died of severe necrotic hepatitis within 2 weeks postinfection, whereas those having received no silica survived for 3 weeks or more after challenge. Silica given day 4 postinoculation had no effect. The virus titers of the liver and spleen at day 4 as well as serum interferon levels at day 2 were much higher in silica-treated mice than those without silica treatment. At day 2 or 3 postinoculation, silica-treated mice were found to have a considerable number of necrotic foci in the liver with some neutrophil and lymphocyte infiltration, and viral antigen was present in the cytoplasm of some hepatocytes around necrotic foci. In contrast, those without silica treatment showed only some necrotic foci with some lymphocyte infiltration. Viral antigen was detected only in a few littoral cells but not in hepatocytes. The role of macrophages in the resistance at early stage of inection in nude mice is discussed.
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PMID:The role of macrophages in the early resistance to mouse hepatitus virus infection in nude mice. 22 88

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


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