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Biomedical subjects

G Hess

Publications and source records attributed to G Hess.

At least 217 records · Page 12Linked to original sources
PubMed1980

Failure to detect naturally occurring serum inhibitors of hepatitis B virus deoxyribonucleic acid polymerase.

Sera of patients with past or ongoing hepatitis -B virus infection were tested for the presence of inhibitors of hepatitis -B virus-specific deoxyribonucleic acid (DNA) polymerase activity. None of the sera tested, which included those from anti-hepatitis B surface- and anti-hepatitis B core antigen-positive hemophiliacs, anti-hepatitis Bc antigen-positive hepatitis B surface antigen carriers, patients with hepatitis B surface antigen-positive chronic active hepatitis, hepatitis B surface antigen-positive hemodialysis patients, tumor patients with minimal hepatitis, patients with acute type B, type A, and type non-A, non-B hepatitis and individuals with autoimmune phenomena, contained inhibitors of DNA polymerase activity. This implies that the DNA polymerase test is not affected when utilized to quantitate DNA-containing Dane particles. In addition, there is no evidence that inhibitors of DNA polymerase activity play some pathogenic role in the course of hepatitis B virus infection.

Carrier State↗
PubMed1980

Autoantibodies against liver-specific membrane lipoprotein in acute and chronic liver diseases: studies on organ-, species-, and disease-specificity.

A double antibody radioimmunoprecipitation test was used to detect anti-human LSP, anti-rabbit LSP, and autoantibodies against the human kidney equivalent of LSP (anti-HKP) in patients' serum. Anti-human LSP was found in 27/62 cases with chronic active liver disease (CALD), 9/16 cases with chronic persistent hepatitis (CPH), and 14/33 patients with acute viral hepatitis (AVH), 2/10 patients with ;inactive' cirrhosis of the liver (Ci), 4/14 patients with alcohol induced liver disease (ALD), 1/7 patients with miscellaneous liver diseases (MLD), and in 6/58 patients with primary non-hepatic autoimmune disease (PNHA). Frequencies of anti-LSP did not depend on HBsAg status. Anti-rabbit LSP was detected in only 9% of patients with AVH as compared with 42% for anti-human LSP. No such difference was observed in the other groups of patients. Anti-HKP was found in 6/62 patients with CALD, 1/7 patients with MLD, and 2/58 patients with PNHA; no anti-HKP occurred in patients with CPH, AVH, ALD, and Ci. The frequency of anti-LSP was not correlated with the presence of non-organ-specific autoantibodies in patients with CALD; furthermore, no correlation with sex-distribution, age, gammaglobulin levels, and SGOT occurred in this group of patients. No correlation existed between anti-LSP and liver membrane autoantibodies detected by indirect immunofluorescence on isolated rabbit hepatocytes (LMA). The reported data show that naturally occurring anti-LSP, characteristic for acute and chronic inflammatory liver diseases, are mostly directed against organ-specific determinants of the LSP complex. It is suggested that the occurrence of antibodies to species-specific determinants of LSP reflects a transient state of autoimmunity. The LMA immunofluorescence test seems to detect antibodies against other liver membrane antigens as well as LSP.

Antibody Specificity↗
PubMed1980

Detection and characterization of liver membrane autoantibodies in chronic active hepatitis by a solid-phase radioimmunoassay.

A solid-phase radioimmunoassay was developed to detect antibodies to liver membrane antigens in sera of patients with HBsAg-negative and -positive liver diseases and primary non-hepatic autoimmune diseases. Ten of fourteen patients with HBsAg-negative CAH had autoantibodies detected by RIA; negative results were obtained with sera of seven patients with HBsAg-positive acute and chronic liver diseases, six patients with miscellaneous liver diseases, including two patients with PBC, two healthy blood donors and seven patients with primary non-hepatic autoimmune diseases. Antibodies detected by RIA correlated with liver membrane autoantibodies (LMA) found by indirect immunofluorescence; no correlation was observed with AMA, ANA and SMA. Species-cross-reacting antibodies could be absorbed by preincubation with isolated plasma cell membranes prepared from rabbit livers. Liver membrane autoantibodies detected by RIA were directed against three different antigen fractions obtained from Sepharose 6B chromatography including LSP and LM-Ag. Only three of ten antibodies were directed against species-specific determinants; others cross-reacted with rabbit antigens. Only the antibody to LSP was organ-specific, all others cross-reacted with kidney proteins. Ferritin, human serum albumin and human plasma lipoprotein were excluded as target antigens. Although several sera reacted with identical molecules a remarkable heterogeneity of liver membrane autoantibodies was observed.

Adult↗
PubMed1980

Hepatitis B virus markers among family contacts and medical personnel of 239 hemodialysis patients.

The present study was initiated to assess the risk of infection of medical personnel and family contacts of hemodialysis patients. It confirms previous reports that hemodialysis patients and staff members of hemodialysis units are at high risk of acquiring HBV infection. Approximately 25% of the household contacts had serological signs of past or ongoing HBV infections. The risk of infection of the family contact was independent of the mode of dialysis but increased if the contact was a spouse, assisted in dialysis, or if the index hemodialysis patient was HBsAg positive. There is an urgent need for active immunization to prevent spread of HBV related to hemodialysis.

Antibodies, Viral↗
PubMed1979

[Spread of hepatitis B virus infection among family contacts of asymptomatic HBsAg carriers (author's transl)].

Family members of 34 asymptomatic HBsAg carriers were tested for different hepatitis B virus (HBV) markers. Among 67 family members tested 24 (36%) presented signs of a past or ongoing HBV-infection. Spread of HBV-infection was particularly high in those families in which the HBsAg carrier was positive for HBeAg and Dane particle-associated DNA polymerase activity. Non-parenteral "horizontal" transmission of HBV among spouses and brothers and sisters and probably parenteral vertical transmission of HBV from carrier mothers to their infants occurred in approximately the same frequency. Fathers transmitted HBV unfrequently to their offsprings. The results show that the risk to acquire a HBV-infection from an asymptomatic HBsAg carrier is closely linked to the serological findings in the HBe/anti-HBe-system of the index HBsAg carrier and not to the family relationship to the HBsAg carrier.

Adolescent↗
PubMed1979

Hepatitis B virus markers in 97 long-term hemodialysis patients.

A study was undertaken to assess the state of hepatitis B virus (HBV) infection in hemodialysis patients. From 97 hemodialysis patients tested, 51 were found to have at least one hepatitis B virus specific marker. 18 were HBsAg carriers, 12 of these carriers have to be regarded as infectious as judged from the presence of HBeAg and/or HBV-specific DNA polymerase activity in the serum. Antinuclear antibodies (ANA) were found in the sera of approximately 20% of the hemodialysis patients with a high prevalence in cases which lacked HBV markers. We conclude from our study that HBsAg-positive hemodialysis patients should be dialyzed in a separate unit and preferably served by personnel which is anti-HBs-positive. The question whether patients in which anti-HBc represents the only HBV marker should be separated is still open and needs further work. The role of non-A/non-B infection is difficult to determine and further studies are needed to elucidate this question.

Adult↗
PubMed1979

Etiology of hepatitis B surface antigen (HBsAg)-negative chronic hepatitis.

A study was undertaken to elucidate the etiology of HBsAg-negative chronic hepatitis. Form 37 individuals with HBsAg-negative chronic hepatitis, 11 had liver membrane autoantibody (LMA) and were thus classified as autoimmune. 6 patients had anti-HBc, 1 of which was also positive for LMA. The majority of individuals with HBsAg-negative chronic hepatitis had antibodies to hepatitis A antigen (anti-HAV), in general at low titer. We conclude from our data that hepatitis A and hepatitis B virus infections are unlikely to play a significant role in inducing or maintaining HBs-Ag-negative chronic hepatitis. The etiological role of non-A non-B hepatitis agent(s) is difficult to estimate and must await the detection of appropriate markers for type non-A non-B hepatitis.

Adult↗
PubMed1979

Hepatitis B virus markers among family contacts of asymptomatic HBsAg carriers.

A study was undertaken to establish the risk of family contacts of HBsAg carriers acquiring a hepatitis B virus (HBV) infection. About one-third of all household contacts of asymptomatic HBsAg carriers had signs of past or ongoing HBV infection. Family contacts of HBsAg carriers with high numbers of circulating Dane particles were shown to have a higher risk of developing HBV infection than family contacts of HBsAg carriers without serological evidence of HBV synthesis. The probability of acquiring HBV infection was not different between spouses, parents, children, and brothers and sisters, respectively of asymptomatic HBsAg carriers.

Adult↗
PubMed1979

[Radioimmunological determination of HBeAg/anti-HBe in HBsAg-positive liver diseases and in "healthy" HBsAg carriers].

This paper describes a "solid-phase"-radioimmunoassay for the demonstration of HBeAg and anti-HBe. The investigations revealed the following results: 1. HBeAg is positive in all patients with acute type B-hepatitis during the acute phase of illness. During the normal course of the disease HBeAg turns to negative followed by an anti-HBe lasting for several months. 2. Cases with a persistent virus B-replication as HBsAg-positive CPH, CAH or patients on hemodialysis are positive for HBeAg in their serum. By means of the fluorescent antibody technique these patients have demonstrable HBcAg and HBeAg in their liver biopsies. 3. Healthy HBsAg carriers are anti-HBe-positive in their serum. In their liver biopsies there are no signs of an on-going virus B-replication (HBsAg and HBeAg negative). 4. The radioimmunological determination of HBeAg and anti-HBe enables us to differentiate between the groups with HBsAg positive acute or chronic hepatitis and the group of healthy HBsAg-carriers.

Antibodies, Viral↗
PubMed1979

Tests for Dane particles in serum concentrates of HBsAg positive hemodialysis patients.

The present study was undertaken to assess the infectivity of sera from HBsAg positive hemodialysis patients by measuring HBeAg, DNA polymerase activity and Dane particle associated HBcAg. Of 33 sera tested 25 were positive for at least one of these tests for Dane particles, indicating that most HBsAg positive hemodialysis patients are highly infectious. The demonstration of DNA polymerase activity in serum concentrates was proven to be the most sensitive assay for the detection and quantitation of Dane particles in serum. We conclude from our results that HBsAg positive hemodialysis patients should be treated in separate units and be served by staff who are either anti-HBs positive or HBsAg carriers.

DNA-Directed DNA Polymerase↗
PubMed1979

Demonstration and partial characterization of 22-nm HBsAg and Dane particles of subtype HBsAg/ady.

The present paper describes the demonstration of d, y, w, and r HBsAg determinants in one serum. It was shown that there are two populations of HBsAg particles: HBsAg/ad and HBsAg/ady. All complete Dane particles were of subtype HBsAg/ady. Further characterization of HBsAg/ady particles did not reveal morphologic differences when they were compared with HBsAg/ad and HBsAg/ay particles. An HBsAg/ady phenotype may be the result of a double infection with hepatitis B viruses or exchanges of DNA sequences that determine HBsAg/ay and HBsAg/ad to form a new genotype.

Adult↗
PubMed1978

Anti-HBc, HBeAg and DNApolymerase activity in healthy HBsAg carriers and patients with inflammatory liver diseases.

In this paper we report on anti-HBc-titers, HBcAg, DNApolymerase activity in the serum and intracellular HBsAg in healthy HBsAg-carriers and patients with HBsAg-positive inflammatory liver diseases. 32/44 patients with acure virus-B-hepatitis were negative for anti-HBc in the first week of the disease. Anti-HBc-titers in healthy HBsAg-carriers varied between 1:10 and 1:32,000 (medium titer 1:4,000). In HBsAg-positive CAH we found a medium titer between 1:32,000 and 1:64,000, in cases with CPH of about 1:16,000. All autoimmune type CAH showed anti-HBc-titers less than 1:10. By immunofluorescence we could demonstrate in a group of 71 asymptomatic HBsAg-carriers in none of the healthy HBsAg-carriers HBcAg in the liver cell nuclei. In contrast HBcAg could only be found in 4/5 HBsAg positive CAH- and 6/9 CPH patients. No elevated DNApolymerase activity could be demonstrated in healthy HBsAg-carriers. Out of 44 patients with virus-B-hepatitis only 3 showed elevated DNApolymerase activity. On the other hand DNApolymerase elevation was demonstrable in 17/37 cases with CAH and 9/15 with CPH. The investigations showed a strong correlation between the demonstration of HBcAg in the serum and the DNApolymerase activity. The characteristic findings enabled us to differentiate between "healthy" HBsAg-carriers and HBsAg-carriers with inflammatory liver diseases.

Alanine Transaminase↗
PubMed1978

Radioimmunoassay for the detection of the antibody against hepatitis-B-core antigen (anti-HBc).

In this paper we describe a new sensitive solid phase radioimmunoassay for the detection of anti-HBc. This test was shown to be more sensitive than the widely used immune adherence hemagglutination test (IAHA) and at least as sensitive as the radioimmunoassay using the blocking principle. The new test system appears to be very useful to screen larger groups of individuals (e.g. blood donors) for the presence of anti-HBc.

Antibodies↗
PubMed1978

Anti-HBc titers in HBeAg and anti-HBe positive asymptomatic HBsAg carriers.

A study was undertaken to establish markers for HBV replication in relation to HBeAg and anti-HBe. HBsAg carriers with serum HBeAg had DNA polymerase activity in the serum and HBcAg in the liver nuclei. Anti-HBe positive and anti-HBe/HBeAg negative sera lacked these markers. For anti-HBc the following geometrical mean titers were calculated: 1: 12,000 for HBeAg positive, 1:9, 100 for anti-HBe and anti-HBc positive, and 1:2,800 for anti-HBc positive anti-HBe/HBeAg negative asymptomatic HBsAg carriers. Follow up studies revealed mostly unchanged anti-HBc titers in all three groups over an observation period of ten to twenty months. Our data argue for a prolonged HBV replication in all HBsAg carrier subgroups compared to individuals with an uncomplicated acute virus-B-hepatitis. This study gives no final answer whether HBeAg negative HBsAg carriers have a continous HBV replication.

Antibodies, Viral↗