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Biomedical subjects

C J Burrell

Publications and source records attributed to C J Burrell.

99 records · Page 6Linked to original sources
PubMed1974

Antibody to hepatitis B antigen in haemophiliacs and their household contacts.

The prevalence of antibody to hepatitis B antigen, detectable by radioimmunoassay, was found to be no higher among 58 long-term household contacts of multiply transfused haemophiliacs than among 100 randomly chosen blood donors. This suggested that such contacts do not have greater exposure to serum hepatitis virus than that occurring through natural means. Among those persons possessing antibody, the multiply transfused haemophiliacs showed a marked tendency for higher antibody titres than their contacts, implying differences in pathogenesis between infection acquired through multiple transfusion and infection acquired naturally.

Aspartate Aminotransferases↗
PubMed1972

Rheumatoid arthritis, rheumatoid factor, and tests for Australia or hepatitis-associated antigen.

False-positive results in tests for hepatitis-associated antigen using latex agglutination techniques may be due to rheumatoid factor in the serum. Possibly the use of IgM antibody in preparing the latex particles might diminish the occurrence of such reactions. No evidence was found for a relation between rheumatoid arthritis and a significant incidence of hepatitis-associated antigen detectable by countercurrent immunoelectro-osmophoresis.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Correlation between liver histology and markers of hepatitis B virus replication in infected patients: a study by in situ hybridization.

Liver sections from 18 patients positive for hepatitis B surface antigen (HBsAg), and from 12 negative patients, were examined for the presence of hepatitis B virus (HBV) DNA using an in situ hybridization assay that would identify only those hepatocytes containing more than 10 to 15 HBV genome equivalents per cell. Such cells are likely to be undergoing active viral replication, rather than latent infection. The findings were correlated with results of tissue immunofluorescence for HBV antigens and the presence of serum hepatitis B e antigen (HBeAg), together with histologic assessment of each liver. HBV DNA detected in the above assay was predominantly cytoplasmic; it was associated with the presence of hepatitis B core antigen (HBcAg) in hepatocytes and HBeAg in serum, and to a lesser extent with cirrhosis and immunosuppression, but not with the presence of HBsAg in hepatocytes, nor with histological evidence of disease activity judged by the presence of piece-meal necrosis and lobular and portal tract inflammation. These findings support the view that liver HBcAg and serum HBeAg are markers of virus replication, and demonstrate that active liver disease in HBsAg-positive patients may occur with or without such markers of replication. It is proposed that alternative mechanisms for hepatocyte injury may apply in different chronic HBV patients, one related to virus replication and one dependent on immunological factors.

Adolescent↗
PubMedDate not supplied

Cellular localization of alpha-interferon in hepatitis B virus-infected liver tissue.

Cells expressing alpha 2-interferon were identified by indirect immunofluorescence using both a polyclonal and a monoclonal anti-alpha-interferon antibody reagent. In hepatitis B or delta virus infection, focal clusters of alpha-interferon-positive infiltrating mononuclear cells and (to a lesser extent) fibroblasts were regularly seen in liver sections from patients who had chronic active hepatitis and cirrhosis and evidence of virus replication, but in a minority of patients with chronic persistent hepatitis B and not in nonvirally infected livers. This report provides evidence for local alpha-interferon production near the site of virus replication in hepatitis B infection, identifies mononuclear cells and fibroblasts (but not hepatocytes) as the main cell types producing interferon in this infection and suggests that locally produced alpha-interferon may be a natural regulator of virus replication in HBsAg-positive chronic active hepatitis. Furthermore, serological characterization of the interferon species produced locally may predict which particular interferon species could be of the greatest therapeutic benefit in specific disease states or individual patients.

Antigens, Viral↗
PubMedDate not supplied

Experimental duck hepatitis B virus infection: pathology and evolution of hepatic and extrahepatic infection.

Seventy, 1-day-old ducklings inoculated intraperitoneally with duck hepatitis B virus and 30 controls have been studied over a 2-year period. Infection with duck hepatitis B virus occurred in all inoculated ducks, although this was not associated with clinical morbidity. Duck hepatitis B virus DNA was first detected in liver on Day 3, in pancreatic acinar cells on Day 4, serum on Day 6, splenic red and white pulp on Day 7 and in the renal glomurulus on Day 14, using a combination of dot, Southern blot and in situ hybridization techniques. Peak levels of circulating virus, as determined by DNA polymerase levels, occurred 1 to 4 weeks postinoculation. Mild degrees of portal inflammation were seen in sections of liver tissue in both infected and control ducks. However, moderately severe inflammatory changes were present in 8 of 22 infected birds compared with 0 of 18 controls (p less than 0.025). Appearance of this inflammatory infiltrate 6 weeks postinoculation coincided with a decrease in levels of duck hepatitis B virus DNA in hepatocytes and within the pancreatic acinar cells. At the same time, duck hepatitis B virus DNA became increasingly localized to the splenic germinal centers, and viral DNA was first detected in pancreatic islet cells. No histological changes accompanied the extra-hepatic tissue infection. The sequence and significance of duck hepatitis B virus infection in liver and extra-hepatic tissues is discussed in relation to the pathogenesis of hepatitis B virus infection in man.

Animals↗
PubMedDate not supplied

Dialysis-associated hepatitis in Edinburgh; 1969-1978.

In 1969-1970 there was a sharp outbreak of hepatitis associated with hemodialysis in two Edinburgh hospitals; mortality was 24% among renal patients and 31% in staff members. The epidemiology of the outbreak, the measures taken to control it, and the efforts made to exclude hepatitis B virus infections during an eight-year period after the outbreak, were reviewed in the light of a retesting of stored specimens by modern diagnostic techniques for hepatitis A and B viruses. This review reveals that the outbreak involved some dual infections with both hepatitis B and non-A, non-B hepatitis viruses and that the occurrence of two infections at once was probably related to the exceptional virulence of the outbreak. The review also reaffirms that the routine serotesting of renal patients and staff members and the dialysis of infected patients in a geographically separate isolation facility are effective methods of controlling the spread of hepatitis B virus in hemodialysis units.

Child↗