Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Catechin derivatives including (-)-epicatechin gallate (ECG), (-)-epigallocatechin gallate (EGCG), (-)-epigallocatechin (EGC) and green tea extract (GTE) were found to inhibit the activities of cloned human immunodeficiency virus type 1 reverse transcriptase (HIV-1 RT), duck hepatitis B virus replication complexes reverse transcriptase (DHBV RCs RT), herpes simplex virus 1 DNA polymerase (HSV-1 DNAP) and cow thymus DNA polymerase alpha (CT DNAP alpha). EGCG and ECG were shown to be very potent inhibitors of HIV-1 RT. According to the IC50 values for HIV-1 RT, these compounds can be ordered as EGCG 0.0066 mumol/L > ECG 0.084 mumol/L > GTE 0.1 microgram/ml > EGC 7.2 mumol/L. DHBV RCs RT was the least sensitive to these compounds. Kinetic study showed that EGCG exerts a mixed inhibition with respect to external template inducer poly (rA).oligo (dT) 12-18 and a noncompetitive inhibition with respect to substrate dTTP for HIV-1 RT. Bovine serum albumin significantly reduced the inhibitory effects of catechin analogues and GTE on HIV-1 RT. In tissue culture GTE inhibited the cytopathic effect of coxsackie B3 virus, but did not inhibit the cytopathic effects of HSV-1, HSV-2, influenza A or influenza B viruses.
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PMID:[The inhibitory effects of catechin derivatives on the activities of human immunodeficiency virus reverse transcriptase and DNA polymerases]. 128 89

293 cases of acute hepatitis occurring within two years were analyzed with regard to type of viral infection, clinical course and outcome. Infections occurring in high risk groups as in drug addicts, transfused patients and medical staff were evaluated separately. Within the "posttransfusion group" there was a relatively high incidence of hepatitis B virus infection, high-lighting the need for more extensive screening of blood products for the hepatitis B virus. The prognosis of the disease was independent of time of stay in hospital, of treatment with beta-Cyanidanol and vitamins and of accidental corticosteroid therapy. The highest prevalence of chronicity was found in the Non-A-Non-B group.
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PMID:[Epidemiology, clinical aspects and prognosis of viral hepatitis A, B and non-A, non-B]. 313 25

The hepatoprotective antioxidant bioflavonoid cianidanol has beneficial therapeutic and immunomodulatory effects in chronic hepatitis. Its action on natural killer (NK) cell activity has not yet been studied in hepatitis B virus (HBV) infection. In the present study, the in vitro and in vivo effects of the drug on NK cell activity have been determined in six patients with chronic HBV hepatitis and in ten healthy control subjects. Two methods were used: an enzyme release assay and a cytotoxicity test based on the assessment of endogenous alkaline phosphatase activity of the target cells. The in vitro effect of the drug was assessed using cianidanol at 10(-6), 10(-5) and 10(-4) M concentrations. For in vivo studies, HBV hepatitis patients were treated with cianidanol at a daily dose of 3.0 g cianidanol for seven days and were investigated before and after the treatment. Chronic HBV hepatitis patients showed a moderate decrease in NK cell activity compared to the controls, but after the cianidanol therapy their NK cell activity significantly rose to 68.0% +/- 9.5% (p less than 0.01). Cianidanol in vitro inhibited the NK cell activity both in hepatitis and healthy groups when using K-562 target cells and the lactic acid dehydrogenase enzyme release assay, but did not influence or even slightly enhance the NK activity when human embryonic fibroblast cells and alkaline phosphatase assay were used for the test. After the 7-day in vivo treatment, the in vitro inhibitory action of the drug was diminished or absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of cianidanol on natural killer cell activity in patients with chronic B virus hepatitis. 359 73

This study was designed to investigate the effect of the natural bioflavonoid compound cianidanol on the blood lipid peroxide status of patients with chronic hepatitis. Nine patients had chronic active liver disease--seven of them hepatitis B virus-positive--and five had chronic alcoholic hepatitis. Besides some biochemical liver function tests (serum bilirubin, aminotransferases and gamma-glutamyl transferase), the changes in the serum level of malondialdehyde (a thiobarbituric acid reactive substance) as one of the end-products of lipid peroxidation, as well as the quantity/or activity of enzymes controlling peroxidation (superoxide dismutase (SOD), glutathione peroxidase and catalase) were measured. In addition, the serum level of the natural antioxidant vitamin E was followed-up. Cianidanol treatment (at a dose of 3.0 g/day for one month and of 1.5 g/day for two months) resulted in a slight improvement in aminotransferases and a significant fall (normalization) of high serum malondialdehyde level. After a marked transient increase, serum SOD content decreased while glutathione peroxidase and catalase activities as well as the vitamin E blood level increased during the treatment. Results suggest that (cianidanol in vivo inhibits lipid peroxidation and influences antioxidant enzyme systems and vitamin E in the blood of patients with chronic hepatitis.
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PMID:Effects of cianidanol on the blood lipid peroxide status in patients with chronic hepatitis. 409 18

It has been shown that (+)-cyanidanol-3, therapeutically administered during the course of acute hepatitis B, is able to favor the elimination of hepatitis B surface antigen (HBsAg) from the blood. This observation suggests that (+)-cyanidanol-3 might stimulate the cell-mediated immune response, since it is known that this type of response is responsible for elimination of the virus. In the present study, the possible action of (+)-cyanidanol-3 on this type of immunity was investigated by adding the substance in vitro to leukocyte migration inhibition tests, performed with the antigens purified protein derivative (PPD) and HBsAg and with leukocytes from individuals sensitized to these antigens. In normal individuals sensitized to PPD, the addition of (+)-cyanidanol-3 amplified the inhibition of migration by 7.0% (P less than 0.05). In patients previously infected by hepatitis B virus and sensitized to HBsAg, the addition of (+)-cyanidanol-3 amplified the migration inhibition by 10.5% (P less than 0.05). A trend to a dose-response relation was observed with the antigen PPD. (+)-Cyanidanol-3 did not modify leukocyte migration in the absence of an antigen. (+)-Cyanidanol-3 therefore seems capable of amplifying the cell-mediated immune response as measured by the leukocyte migration inhibition test. It is thus possible that it favors the elimination of HBsAg in patients by this mechanism.
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PMID:Influence of (+)-cyanidanol-3 on the leukocyte migration inhibition test carried out in the presence of purified protein derivative and hepatitis B surface antigen. 725 Nov 31