PubMed Health⌕ Search

Biomedical subjects

A J Zuckerman

Publications and source records attributed to A J Zuckerman.

At least 19 recordsLinked to original sources
PubMed1992

Toga virus-like particles in acute liver failure attributed to sporadic non-A, non-B hepatitis and recurrence after liver transplantation.

Toga virus-like particles (typically 60-70 nm: enveloped with small surface spikes) were detected in the native hepatectomy specimens in 7 of 18 patients grafted for acute liver failure attributed to sporadic non-A, non-B hepatitis and in 2 patients grafted for fulminant hepatitis attributed to anti-epileptic drug hepatotoxicity. These particles were not detected in the hepatectomies from 12 other patients grafted for other causes of acute liver failure, 12 for various chronic liver diseases, and 2 histologically normal livers. Acute hepatic failure, characterized histologically by severe haemorrhagic necrosis, developed 7 days after grafting in 5 patients, all in the non-A, non-B group with toga virus-like particles in native liver. Similar virus-like particles were detected in all grafts and were in greater abundance than in the native livers. The agent may be novel because pre- and post-grafting sera were negative for antibodies against representative panels of arboviruses and in first and second generation antibody tests for hepatitis C virus.

Adolescent↗
PubMed1992

Improved diagnosis of chronic hepatitis C virus infection by detection of antibody to multiple epitopes: confirmation by antibody to synthetic oligopeptides.

Serum samples from 226 patients covering a wide spectrum of liver disease were tested for antibodies to hepatitis C virus (HCV) using both first and second generation enzyme linked immunosorbent assays. Selected sera were also tested by peptide immunoassays, by the four-antigen recombinant immunoblot assay (RIBA II), and for viral genome by the polymerase chain reaction. Antibody to c100-3 was detected in 61% of patients with chronic non-A, non-B (NANB) hepatitis and/or 46.5% with presumed NANB-related cirrhosis by the first generation test. These figures increased to 77% and 58% when antibodies to recombinant structural and non-structural HCV antigens were sought by the second generation assay. Supplemental testing against peptide Sp75 and Sp65/sp67 confirmed that reactivity of sera by second generation assays was due to antibodies to the additional structural and non-structural antigens. Samples negative by the first generation assay were not confirmed by the supplemental assay using peptides Sp75 and Sp65/Sp67. HCV RNA was detected in 60% of the anti-HCV positive sera tested, most of which were also RIBA II positive. Our findings confirm that the introduction of the structural and non-structural antigens, especially the putative nucleocapsid protein, improves sensitivity of detection of antibodies to HCV, and facilitates diagnosis in patients with "cryptogenic" chronic hepatitis.

Antigens, Viral↗
PubMed1992

Assessment of inactivation of hepatitis A vaccine by compound PCR.

Assuring the complete inactivation of hepatitis A virus (HAV) vaccine commonly requires prolonged tissue culture amplification, followed by detection of virus antigen in cell lysates. A reliable, but faster, alternative procedure is highly desirable since it will permit the prescreening of experimental batches of killed HAV, prior to tissue-culture amplification. We established experimental conditions for simultaneous, polymerase chain reaction (PCR)-based amplification of viral and cellular mRNA sequences from infected cell RNA (compound PCR). Under these conditions, the presence of virus-specific amplified sequences, as detected by Southern blot, allows the identification of incompletely inactivated vaccine batches with a threshold practically identical to that of the more time-consuming subculture and ELISA. Compound PCR is, by its nature flexible enough for adaption to different requirements and it should prove useful for rapid prescreening of vaccine batches and pilot studies for improvement of inactivation protocols.

Base Sequence↗
PubMed1979

De novo acute infection and reactivation of hepatitis B virus in established cirrhosis.

Five patients with cirrhosis proved by biopsy had clinical, biochemical, and serological evidence of an acute hepatitis B infection. In two the illness was fulminant and led to death. Only one patient completely recovered. Serological markers for the hepatitis B virus were absent before the onset of the acute illness in four patients, which suggested that a de novo infection had been acquired as a result of recent transfusions of blood or blood products. The fifth patient, who had Goodpasture's syndrome, had antibody to the core of hepatitis B virus, indicating previous exposure to the virus; his acute hepatitis may have been related to immunosuppressive drug treatment, which may have reactivated a dormant virus infection. Thus an acute type B viral hepatitis due to either a de novo or a reactivated infection may be superimposed on cirrhosis.

Acute Disease↗
PubMed1979

Epidemic hepatitis B caused by commercial human immunoglobulin.

An epidemic of acute hepatitis B followed the administration of human immunoglobulin to members of the staff of a mission hospital in India and their families. Jaundice developed in 123 (38%) of 325 persons inoculated. Hepatitis-B surface antigen was detected in three of the batches of immunoglobulin which were available for testing.

Counterimmunoelectrophoresis↗
PubMed1979

Non-A non-B hepatitis associated with chronic liver disease in a haemodialysis unit.

To clarify the aetiology of an outbreak of HBsAg-negative acute hepatitis in the renal unit at Fulham Hospital in 1968--70, serological tests for antibody to hepatitis-A virus (anti-H.A.V.) were done retrospectively on serum samples obtained at the time of the outbreak. 7 patients had had two previous episodes of clinical HBsAg-negative hepatitis. Serum samples were available from 24 of the 29 infected patients, and these were paired in 12 instances. There was a slight increase in the titre of anti-H.A.V. in 1 patient, and a further 2 patients who subsequently developed chronic hepatitis showed a decrease in titre, but no changes in titre were detected in the remaining 21 cases. These findings do not provide evidence for the involvement of hepatitis-A virus in the outbreak of hepatitis and effectively exclude a role for this virus in the chrnoic liver disease which developed subsequently in 8 (28%) of the patients. This outbreak is therefore probably non-A non-B hepatitis, which has not been reported previously in Great Britain in a haemodialysis unit. The results confirm that this form of hepatitis may be related to a high frequency of persistent hepatic dysfunction.

Antibodies, Viral↗
PubMed1979

Transmission of non-A non-B hepatitis to chimpanzees by factor-IX concentrates after fatal complications in patients with chronic liver disease.

6 cases of non-A non-B hepatitis which followed administration of four different batches of concentrates of coagulation factor IX from commercial and non-commercial sources are described. Of 17 patients who received the concentrate on account of chronic liver disease, 4 developed hepatitis, and in 3 of these the illness proved fatal. The incubation periods ranged from 42 to 103 days (mean 65 days). 3 chimpanzees were inoculated with concentrate from the same batch used on the above patients, a further commercial batch upon which no adverse reactions had been reported, and plasma from a known non-A non-B carrier. All developed hepatitis after 10 weeks' incubation. Liver biopsy when serum-aminotransferase was at its highest level showed features consistent with acute hepatitis. As in the patients, viral markers for hepatitis A and B, cytomegalovirus, and Epstein-Barr virus were unchanged.

Acute Disease↗
PubMed1979

The separation and analysis of hepatitis B e antigen.

A solid-phase radioimmunoassay has been used successfully for detecting hepatitis B e antigen in fractionated hepatitis B virus-containing serum. Ammonium sulphate precipitation followed by gel filtration through a column of Sepharose CL-6B resulted in two fractions of antigen-containing material with molecular weights of 220,000 and 130,000. The smaller of these two fractions was found to possess an average isoelectric point of 4.9 and consisted of two major polypeptide species with estimated molecular weights of 66,000 and 17,000 respectively. Affinity chromatography on Blue Sepharose showed that e antigen was not retained under conditions which bound serum albumin. These results are discussed in relation to the immunopathogenesis of hepatitis B.

Carrier State↗