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Biomedical subjects

A J Zuckerman

Publications and source records attributed to A J Zuckerman.

At least 91 records · Page 5Linked to original sources
PubMed1987

Suramin treatment for chronic active hepatitis B--toxic and ineffective.

Suramin has recently been shown to inhibit the activity of the duck hepatitis B virus DNA polymerase (DHBV DNAp) in vitro. However, we found no demonstrable in vivo suppression of human hepatitis B virus DNA polymerase (HBV DNAp) activity in three male patients with severe chronic active hepatitis. Suramin treatment resulted in prolongation of the prothrombin time in all cases and a rise in bilirubin in two and it may have led to haemorrhage from oesophageal varices in one patient and to hepatic encephalopathy in another. Its use in chronic hepatitis is not recommended.

Esophageal and Gastric Varices↗
PubMed1987

Dynamics and impact of perinatal transmission of hepatitis B virus in North India.

The magnitude and significance of perinatal transmission of hepatitis B virus (HBV) were assessed in infants of 8,575 women, of whom 3.7% were seropositive for HBV surface antigen (HBsAg). The e antigen of HBV (HBeAg) was found in 7.8% of these carriers, the antibody to HBeAg (anti-HBe) was found in 30.1% of them, and HBsAg alone was found in 62.1% of them. The estimated incidence of HBsAg positivity by 6 months of age in infants of carrier women was significantly (P less than .001) higher than in controls (18.6% vs 3.0%). Transmission was most frequent (87.5%) if the carrier mother was HBeAg positive and was much less so if she was positive for anti-HBe (17.5%) or for HBsAg alone (9.6%). Toward the end of infancy incidence of HBsAg positivity among offspring of carriers and among controls was not different. Most infants positive for HBsAg and HBeAg continued with the infection beyond 6 months of age. It is estimated that about one-third of the adult asymptomatic HBV carriers in India evolve directly from perinatal infection, while the majority become infected during childhood or early adulthood.

Adolescent↗
PubMed1987

Microbial structures in a patient with sporadic non-A, non-B fulminant hepatitis treated by liver transplantation.

Double-shelled virus-like particles (60 nm) and long cytoplasmic tubular structures were found in the cytoplasm of hepatocytes from areas of collapsed and regenerating areas of hepatectomised liver in a 13-year-old boy who received a liver graft for fulminant hepatitis attributed to sporadic non-A, non-B hepatitis. The patient died on the ninth postoperative day from acute graft failure. Although virus-like particles were not found, instead, gram-negative rods were identified in the necrotic graft and the most likely cause of death was a gram-negative septicaemia with a Shwartzman-like reaction localized to the liver.

Adolescent↗
PubMed1987

Mechanisms of liver cell damage in acute hepatitis B.

Markers of hepatitis B viral infection and the evolution of immune response to these were compared with serum alanine aminotransferase (ALT) levels in adult male and non-pregnant and pregnant female patients with acute hepatitis B from the time of onset of disease to the seventh week. In the adult male and non-pregnant female patients, the peak ALT levels of about 360 IU/litre, seen at the time of onset, gradually declined during the course of the disease. Significantly, even in the seventh week, the median ALT level was abnormal (80 IU/litre). In contrast, the disease was mild in pregnant patients and the ALT levels declined rapidly, returning to normal by the third week. Markers associated with HBV replication, i.e., serum HBV-DNA and HBeAg, declined early in the course of the disease in both groups. The anti-HBc-IgM and anti-HBe responses were well evolved early in the course of the disease in both groups. HBsAg was present in the serum in large amounts (1-1.5 X 10(4) AU/100 microliter) early in the course of the disease and remained so up to the seventh week. Even the pregnant patients who had recovered clinically by the fourth week continued to have HBsAg in their sera in large amounts in spite of normal ALT levels. LMI and LTT responses to HBsAg, which were practically absent in the first week, gradually increased to a peak during the fourth week and remained elevated up to the seventh week in adult male and non-pregnant female patients. In contrast, LMI response to HBsAg was absent in pregnant patients with acute hepatitis B even up to the fourth week Thus, continued liver cell necrosis after the fourth week, as indicated by raised ALT levels, may be associated with T cell responses to HBsAg.

Acute Disease↗
PubMed1987

Virological markers and antibody responses in fulminant viral hepatitis.

Clinical profiles, serological markers, and antibody responses to antigens of hepatitis B virus (HBV) were studied in patients with fulminant viral hepatitis. Whereas hepatitis A and B were found to be uncommon causes (6.9% and 12.2%, respectively), non-A, non-B (NANB) hepatitis was found to be the most common cause of fulminant hepatitis (80.9%). As against this, the incidence of hepatitis B and NANB hepatitis was very similar in nonfulminant acute viral hepatitis in adults (41.2% and 51.9%, respectively). Pregnancy with labour was an important precipitating factor for development of fulminant hepatitis of the NANB type only; 32% of fulminant NANB hepatitis patients were pregnant women and 22.6% had a history of labour preceding hepatic coma. Only 0.8% of nonfulminant NANB hepatitis cases were pregnant women. Another major precipitating factor for the development of the fulminant form of NANB hepatitis was concomitant chronic HBV carrier state. A total of 38.6% of fulminant NANB hepatitis patients were HBV carriers, whereas only 19.2% of nonfulminant acute NANB hepatitis cases were HBV carriers. Sera of 32 chronic HBV carriers with fulminant NANB hepatitis and 10 cases of fulminant hepatitis B were tested for delta antibody, and all were nonreactive. The antibody responses of the fulminant hepatitis B patients to the antigens of HBV were found to be greater compared to those of patients with nonfulminant acute hepatitis B. Antibody responses of chronic HBV carriers with fulminant NANB hepatitis to antigens of HBV were found to be depressed in comparison with those of chronic asymptomatic carriers.

Acute Disease↗
PubMed1987

Screening of antiviral drugs for hepadna virus infection in Pekin ducks: a review.

Acyclovir and suramin were examined for their efficacy alone and in combination, against duck hepatitis B virus (DHBV) in persistently infected Pekin ducks. The pharmacokinetics of acyclovir in ducks showed that the peak plasma concentration was reached 30 min after oral administration. Oral acyclovir and suramin administered intravenously suppressed the replication and production of infectious virions as measured by marked reduction of DNA polymerase activity during treatment. However, rebound of enzyme activity was observed soon after cessation of drug therapy. In contrast, sustained reduction of polymerase activity was attained by combined therapy of acyclovir followed by suramin, demonstrating a significant enhancement of anti-DHBV activity which requires confirmation in a larger experimental study. This report reviews the work with the duck model, demonstrating that it is ideal for screening antiviral compounds for treatment of infection with hepadna viruses.

Acyclovir↗
PubMed1987

Tomorrow's hepatitis B vaccines. Arie Zuckerman discusses hepatitis B vaccines of the future and the impact of AIDS on immunization.

Recombinant hepatitis B vaccines produced in yeast and in mammalian cells are the first of future vaccines against this important public health problem. Hybrid virus vaccines and the use of baculoviruses for expression of hepatitis B antigens in insect cell cultures will follow shortly and chemically synthetic vaccines are under development. The impact of AIDS on future immunization programmes should be considered.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Randomised controlled trial of lymphoblastoid interferon for chronic active hepatitis B.

Thirty male patients (27 homosexual) with biopsy proven chronic active hepatitis B were randomised to receive lymphoblastoid interferon (Wellferon) or no treatment. All patients were HBeAg positive and had continuing viral replication. Patients receiving treatment were given a single daily intramuscular injection of interferon for 28 days at a starting dose of 2.5 MU/m2 increasing to a maximum of 7.5 MU/m2/day. Transient side effects of malaise and influenza like symptoms occurred in all patients and resolved rapidly after treatment. Hepatitis B viral replication was suppressed during interferon treatment in all patients but the effect was limited to the period of therapy. After one year there was no appreciable difference in viral markers between the two groups of patients and this treatment schedule appears less effective than the thrice weekly, three month regimes recently reported from other centres.

Adult↗
PubMed1987

Hepatitis B virus chronic liver disease and hepatocellular carcinoma.

Numerous studies have shown the presence of a highly significant excess of HBsAg, core and surface antibody in patients with hepatocellular carcinoma (HCC). An important factor in the aetiological association between hepatitis B and HCC may lie in the early age of infection. Although hepatitis B virus (HBV) DNA has been found in HCC tissue, there is no simple correlation between serum markers of hepatitis B infection and viral DNA in the tumour. Nevertheless, it is clear that in the case of HBV-associated HCC, integrated HBV sequences may be present in more than 80% of the tumours. The possible molecular basis for the resulting neoplastic transformation is discussed. Whatever the molecular basis of HBV involvement in the causation of HCC, immunization against HBV is likely to prevent primary liver cancer.

Carcinoma, Hepatocellular↗
PubMed1987

The development of novel hepatitis B vaccines.

Development of vaccines against viral hepatitis B has proceeded along four main lines. (1) Human plasma-derived vaccines are safe, effective and are now in general use. (2) Subunit polypeptide vaccines formulated in micelles have reached the stage of clinical trials. (3) Recombinant DNA vaccines have been produced in prokaryotic and eukaryotic cells, notably in yeast. The yeast-derived recombinant vaccines have proved safe and effective in extensive clinical trials, eliciting antibodies which in quantity and specificity are equal to those elicited by plasma-derived vaccine. DNA recombinant has also been applied to the development of hybrid and vaccinia virus vaccines which are capable of immunological "priming", and other hybrid virus vaccines are under development. (4) Finally, chemical synthesis has succeeded in producing small peptides which include specific epitopes eliciting antibody responses in experimental animals. Such chemically synthesized preparations offer a prospect of ultimately producing multivalent synthetic vaccines against several viruses, bacteria and protozoa.

Hepatitis B↗
PubMed1987

The development of novel hepatitis B vaccines.

The development of vaccines against hepatitis B has proceeded along four main lines. (i) Human plasma-derived vaccines are safe, effective, and in general use. (ii) Subunit polypeptide vaccines formulated in micelles have reached the stage of clinical trials. (iii) Recombinant DNA vaccines have been produced in prokaryotic and eukaryotic cells, notably in yeast. The yeast-derived recombinant vaccine has proved safe and effective in extensive clinical trials, eliciting antibodies of equal quantity and quality of specificity to those elicited by plasma-derived vaccine. DNA recombination has also been applied to the development of hybrid vaccinia virus vaccines which are capable of immunological 'priming'. (iv) Finally, chemical synthesis has succeeded in producing small peptides which include specific epitopes eliciting antibody responses in experimental animals.

Cloning, Molecular↗
PubMed1986

AIDS and insects.

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗
PubMed1986

AIDS in primates.

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Acquired Immunodeficiency Syndrome↗