Search PubMed⌕ Search

Biomedical subjects

G Hess

Publications and source records attributed to G Hess.

At least 199 records · Page 11Linked to original sources
PubMed1981

Quantitation of HBeAG and anti-HBe by RIA in sera of chronic HBsAG carriers and individuals with type B hepatitis.

This paper gives the results for HBeAg and anti-HBe titers in chronic HBsAg carriers and patients with type B hepatitis using a "solid-phase" radioimmunoassay. In tumor and hemodialysis patients the HBeAg titers are statistically significant higher compared to the group of HBsAg positive CAH or CPH. High anti-HBe titers are a characteristic finding in "healthy" HBsAg carriers. On the other hand, there is a subgroup of HBsAg positive CAH with anti-HBe; although there are signs of an ongoing virus B replication these cases of CAH proceed sometimes to cirrhosis.

Acute Disease↗
PubMed1981

Hepatitis-B virus-associated deoxyribonucleic acid polymerase: a partial characterization by the use of chemical agents.

The very limited coding capacity of the HBV-DNA led us to study the nature of the HBV (Dane particle) -- associated DNA polymerase. The HBV-associated DNA polymerase met in many respects the characteristics of the repair enzyme of the host: the DNA polymerase beta. It operates under high salt conditions, and exhibits similar salt effects with NaCl, KCL, and PO4(3-). It is insensitive to sulfhydryl group blockers, such as p-hydroxymercuribenzoate and N-ethylmaleimide, is resistant to phosphonoacetic acid, and not inhibited by 5 mol/l urea. It requires a divalent cation (Mg2+) for activity, the Mg2+ concentration revealing optimal activity is somewhat higher than that described for most DNA polymerases beta. The HBV-associated DNA polymerase differs also from most DNA polymerase beta in its sensitivity ot ddTTP and its optimal pH. The fact that DNA polymerase beta of different origin vary considerably in their response to chemical agents and that the DNA polymerase beta from human liver has not been studied allows no definite conclusion as to the nature of the Dane particle-associated DNA polymerase.

Chemical Phenomena↗
PubMed1981

Demonstration and partial characterization of an intermediate HBcAG (Dane particle) population.

Hepatitis-B core antigen (HBcAg) was released from Dane particles previously separated from anti-HBc by repeated pelleting through sucrose gradients separated into three HBcAg populations when analysed by cesium chloride density gradient centrifugation. Heavy HBcAg particles banded at a density of 1.355 gm/ml, intermediate HBcAg particles at a density of 1.33 gm/ml, and light mediate HBcAg particles at a density of 1.30 gm/ml. Like heavy HBcAg particles, intermediate HBcAg particles contained DNA polymerase activity, but the ratio of HBcAg to DNA polymerase activity was significantly different in both populations. Intermediate HBcAg particles could not be separated from heavy HBcAg particles by rate sedimentation centrifugation. The size of the HBV-DNA and the size of its single-stranded gaps were not significantly different in heavy and intermediate HBcAg populations. Data accumulated in this paper suggest that the intermediate HBcAg particle differs from the heavy HBcAg particle by the amount of HBcAg polypeptides and the number of HBcAg determinants exhibited.

Centrifugation, Density Gradient↗
PubMed1981

The significance of serologic, histologic, and immunohistologic findings in the prognosis of 88 asymptomatic carriers of hepatitis B surface antigen.

Eighty-eight asymptomatic carriers of hepatitis B surface antigen (HBsAg) were followed with biochemical, serologic, histologic, and immunohistologic studies over a period of four years. None of the 78 HBsAg carriers with normal or minimally changed liver tissue, antibody to hepatitis B e antigen (HBeAg) in serum, and no intranuclear hepatitis B core antigen (HBcAg) developed a chronic inflammatory liver disease. Four individuals lost circulatory HBsAg, and at least two individuals terminated their HBsAg carrier state. Seven asymptomatic HBsAg carriers with chronic hepatitis were characterized by HBeAg in serum and intranuclear HBcAg. However, three HBsAg carriers with chronic hepatitis and an absence of intrahepatocellular HBcAg were positive for antibody to HBeAg over the observation period. The mechanism that leads to chronic hepatitis in these patients remains to be determined.

Adult↗
PubMed1981

Significance of antibody to hepatitis Be antigen (anti-HBe) in HBsAg-negative individuals.

A study was initiated to assess the significance of antibody to hepatitis Be antigen (anti-HBe) in HBsAg-negative individuals. Anti-HBe was demonstrated in the majority of sera positive for anti-HBs and anti-HBc. All sera positive for anti-HBs and negative for anti-HBc and most sera positive for anti-HBc but negative for anti-HBs were anti-HBe-negative. This implies that the antibody response to HBeAg is of shorter duration than that to HBsAg and HBcAg. Anti-HBe may help to discriminate between various states of hepatitis B virus infection found to be associated with anti-HBc-positive but HBsAg- and anti-HBs-negative sera. 2 individuals were anti-HBe-positive but HBsAg-, anti-HBs- and anti-HBc-negative, this finding is not understood.

Antibodies, Viral↗
PubMed1981

Inhibition of hepatitis B virus deoxyribonucleic acid polymerase by the 5'-triphosphates of 9-beta-D-arabinofuranosyladenine and 1-beta-D-arabinofuranosylcytosine.

9-beta-D-Arabinofuranosyladenine (ara-A), 1-beta-D-arabinofuranosylcytosine (ara-C), and their 5'-triphosphates (ara-ATP and ara-CTP) were tested for ability to inhibit the hepatitis B virus (HBV)-associated deoxyribonucleic acid (DNA) polymerase. Ara-C did not inhibit the HBV DNA polymerase at the concentrations tested, ara-A did so by 50% at a concentration of 30 mM, with the inhibition noncompetitive with respect to deoxyadenosine 5-triphosphate (dATP). Ara-ATP and ara-CTP inhibited the DNA polymerase test competitively with respect to dATP and dCTP, respectively. Both compounds were also active after initiation of the DNA polymerase reaction. The inhibition caused by ara-ATP and ara-CTP was shown to be reversible, with no evidence that ara-ATP or ara-CTP was incorporated into the HBV DNA.

Arabinofuranosylcytosine Triphosphate↗
PubMed1981

Follow-up of anti-HBc titers in healthy HBsAg carriers and patients with chronic inflammatory liver diseases.

Sera of 85 asymptomatic HBsAg carriers found among blood donors were tested for anti-HBc titers and were retested 4 years later. The results were correlated with the histological findings of first and final biopsy. None of 75 HBsAg carriers with normal or minimally changed liver tissue, 71 of them anti-HBe positive, developed chronic inflammatory liver disease. 4 HBsAg carriers eliminated HBsAg from the serum after a 1-to 3-year HBsAg-carrier state and 2 developed antibody against HBsAg in the sequel. In 65 of 75 cases we found unchanged anti-HBc titers. The geometrical mean titer (GMT) was 1:7,800 in the first and 1:7,000 in the final examination with a range of 1:400 and 1:25,600 in the group of HBsAg carriers with normal liver, and was 1:14,200 and 1:10,300, respectively, with a range of 1:800 and 1:51,200 in HBsAg carriers with minimal changes. In both groups the decrease of anti-HBc concentration within 4 years was not significant. The group of 10 HBsAg carriers with chronic hepatitis did not differ from healthy HBsAg carriers in respect to anti-HBc titers. Anti-HBc titers varied between 1:6,400 and 1:25,600, the GMT was 1:13,700 and 1:12,800, respectively. It is speculated that in healthy HBsAg carriers shedding of serologically undetectable quantities of complete and/or defective HBcAg from liver cell nuclei which contain HBcAg not detectable by immunofluorescence maintain the production of anti-HBc.

Antibodies, Viral↗
PubMed1981

[Inhibition of hepatitis B virus associated DNA polymerase by antiviral agents: in vitro studies with clinical implications (author's transl)].

The complete hepatitis B virus (Dane particle) contains a circular doublestranded DNA with single stranded regions and an endogenous DNA polymerase. The HBV associated DNA polymerase closes the single stranded regions of the HBV-DNA in the presence of triphosphatase and a detergent. The DNA polymerase reaction can be inhibition by antiviral substances that exhibit different mode of actions: intercalating agents, phosphonoformiate and the triphosphates of arabinofuranosyladenine and arabinofuranosylcytosine. The value of these in vitro test for the therapy of HBsAg positive chronic liver disease is limited by the fact that is remains so far unclear whether the HBV associated DNA polymerase is a virus- or a host-coded enzyme, and whether virus- or host-coded enzymes are involved in HBV-DNA synthesis in vivo.

Antiviral Agents↗
PubMed1981

Transmission of hepatitis-B-virus by pleural effusion containing Dane particles.

Hepatitis-B-surface antigen HBSAG), hepatitis B-e antigen (HBe(HBeAG), and anti-HBc and Dane particles were demonstrated in pleural effusion obtained from an individual with a protracted course of an acute type B hepatitis, Pleural effusion was found to be unrelated to hepatitis-B-virus (HBV) infection. A physician who injured herself with a needle contaminated with pleural effusion experienced asymptomatic acute type B hepatitis.

Adult↗
PubMed1980

Comparison of indicators for dane particles.

The Dane particle is-because of its characteristics--believed to be the complete hepatitis-B-virus. Sera containing high numbers of Dane particles were shown to be highly infectious. In the present study we related the HBeAg-, the HBsAg- and the anti-HBc titer to the level of DNA polymerase activity measured in 20 fold Dane particle concentrates. The data obtained indicate that the HBeAg concentration gives a semiquantitative estimate on the number of circulating Dane particles. Mean DNA polymerase activity was found to increase with HBsAg concentration and is therefore also of value-if determined in a HBeAg positive serum- for quantitation of Dane particles. The anti-HBc titer was found to be unrelated to the number of circulating Dane particles.

DNA-Directed DNA Polymerase↗
PubMed1980

Inhibition of hepatitis-B-virus DNA polymerase by phosphonoformate: studies on its mode of action.

Phosphonoformate (PFA) and phosphonoacetate (PAA) were tested for their ability to inhibit the hepatitis-B-virus associated DNA polymerase. The HBV DNA polymerase was inhibited by 100 microM/liter PFA 50% while it was highly resistant to PAA. The inhibition of the Dane particle-associated DNA polymerase by PFA was not competitive to substrates and not affected by changes in the magnesium concentration. PFA was active also after initiation of the DNA polymerase reaction. Competition studies revealed that PFA had a higher affinity to a proposed pyrophosphate binding site than PAA or--alternatively--that both compounds bind to different sites.

DNA-Directed DNA Polymerase↗
PubMed1980

Inhibition of hepatitis B virus specific DNA polymerase by intercalating agents.

Intercalating agents, some of them in clinical use, were tested for their ability to inhibit the hepatitis B virus specific DNA polymerase reaction. Ethidium bromide was shown to be the strongest inhibitor among the compounds tested. Compounds in clinical use inhibited the DNA polymerase test only at high concentrations. The inhibitory activity of all compounds tested was increased when the MgCl2 content in the reaction mixture was lowered. UV absorption studies presented no evidence that this effect was due to complex formation of magnesium and the individual compounds. The therapeutic significance of these findings is not certain and needs further work.

Carrier State↗
PubMed1980

The clinical relevance of the antibody to hepatitis B core antigen (anti-HBc): a review.

The antibody against the core component of the Dane particle (anti-HBc) is generally detected in the sera of individuals with acute type B hepatitis and in chronic HBsAg carriers. While the serological demonstration of HbsAg with or without anti-HBc indicates continued replication of viral antigens, the co-occurrence of anti-HBs and anti-HBc is considered a marker of recent HBV replication. The demonstration of anti-HBc in the absence of HBsAg and anti-HBs is in agreement with at least four different states of HBV infection. As this pattern indicates persistent HBV infection in some cases and recovery from an acute type B hepatitis in others, current efforts focus on further characterization of this pattern, using additional test methods such as anti-HBe and anti-HBc of the IgM class.

Acute Disease↗