Publications by authors named "Purcell R"

69 serum pairs from two common-source water-borne outbreaks and one series of endemic cases of hepatitis in three parts of India were tested for hepatitis A and hepatitis B virus infections. None of the patients had evidence of HAV infection and only 10.1% had evidence of HBV infection.

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The hepatitis B virus-associated beta antigen was found in the serum of experimentally infected chimpanzee as an internal component of a discrete subpopulation of hepatitis B surface antigen (HBsAg) particles. The 35- to 37-nm particles banded in CsCl at 1.24-1.

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The epidemiology of infection with the hepatis-B-virus (HBV)-associated delta agent was assessed from the prevalence of antibody to delta in 1206 HBsAg-seropositive subjects from various parts of the world. Anti-delta was prevalent in unselected HBsAg-positive Italians, whether residents in Italy or elsewhere, and in drug addicts and polytransfused HBsag carriers throughout the world, suggesting that delta-associated infection is spread through contact in Italy and parenterally in other countries. Parenteral transmission of the delta agent was confirmed by a separate survey of the prevalence of anti-delta in 648 polytransfused patients with chronic blood disorders, which showed a higher prevalence of anti-delta in HBsAg-positive haemophiliacs than in the general HBsAg-positive population of Italy, Germany, and the U.

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Several subunit vaccines against hepatitis B virus (HBV) have been developed and either are being evaluated or soon will be evaluated for their ability to prevent HBV infection in humans. Most of these preparations consist of highly purified, 22-nm spherical particles of hepatitis B surface antigen (HBsAg) that have been extracted from the plasma of chronic carriers of HBV and inactivated with formalin. Extensive testing in humans and chimpanzees showed these vaccines to be free of residual HBV or other harmful agents and to be capable of stimulating the production of protective antibodies to HBsAg in the majority of recipients.

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Inoculation of hepatitis B surface antigen (HBsAg)-positive sera from patients with chronic liver disease and intrahepatic delta (delta) into chimpanzees susceptible to infection with hepatitis B virus (HBV) resulted in type B hepatitis and delta markers (delta antigen and antibody to delta) in recipient animals. A dilution (10(-8)) of serum induced type B hepatitis without delta markers in another HBV-susceptible animal. HBV infection and delta markers did not develop in animals with preexisting titers of antibody of HBsAg.

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A total of 12 seronegative marmosets (Saguinus mystax) were inoculated orally with hepatitis A virus (HAV) and sacrificed at 3- to 4-day intervals. Tissues from the livers, intestines, mesenteric lymph nodes, and spleens were obtained for immunofluorescence studies, and bile and intestinal contents were obtained for enzyme-linked immunosorbent assay studies. Two marmosets sacrificed on days 34 and 41 after inoculation developed antibody to HAV and demonstrated HAV in their livers but not in any part of their intestinal tissues.

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In a 4-month period, 216 cases of acute viral hepatitis were diagnosed in adults at the Infectious Diseases Hospital, Athens, Greece. Twenty-six percent of these were hepatitis B surface antigen negative. A full set of clinical specimens was obtained from 19 of these patients, who were studied in depth for the etiology of their hepatitis.

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A sensitive "Farr" assay, utilizing 125I-labelled DNA was developed for detecting antibody to single-stranded DNA (anti-ssDNA). The test was shown to be specific and as sensitive as assays using 14C-labelled DNA, for the detection of antibody in patients with connective tissue diseases. Groups of sera from patients with naturally acquired viral hepatitis and experimentally infected chimpanzees were tested for anti-ssDNA by the 125I assay and by counterimmunoelectrophoresis (CIEP).

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Serological investigations for hepatitis B surface and e antigen, antibody to hepatitis B surface, core and e antigen and antibody to hepatitis A virus were carried out in 22 patients with fulminant hepatitis admitted to Medical Department A, Rigshospitalet, Copenhagen, in 1970-77. Nine patients had hepatitis type B and four type A. One patient had evidence of both type A and B infection, whereas the remaining eight patients showed no evidence of type A or B infection.

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In 19 patients followed from biopsy-verified acute viral hepatitis to chronic active liver disease and 74 patients followed to complete resolution verified by a normal liver biopsy, sera from the acute phase were studied for serologic evidence of hepatitis type A and B. Eleven of the 19 patients who developed chronic active liver disease progressed from acute hepatitis type B and 7 from acute hepatitis type non-A non-B. One patient could not be classified because the sera were exhausted.

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A microtitre solid-phase blocking radioimmunoassay (RIA) for antibody to the hepatitis B virus (HBV)-associated delta antigen was specific and detected anti-delta antibody at dilutions of serum of up to 10(6). Analysis of sera from HBsAg-negative subjects and different categories of HBsAg carriers from different regions confirmed the association of anti-delta antibody with HBV infection. Anti-delta antibody was detected in persistently high titres in 19.

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Antibodies to polymerized human albumin (poly-HSA) could not be detected by using sensitive methods (enzyme-linked immunosorbent assay and radioimmunoprecipitation) in sera from chronic carriers of hepatitis B surface antigen (HBsAg) or in serial bleedings from one chimpanzee infected with type A hepatitis virus and one infected with non-A, non-B hepatitis virus. By a solid-phase radioimmunoassay, receptor sites for poly-HSA could be detected on HBsAg particles from sera containing either hepatitis B "e" antigen (HBeAg) or anti-HBe. Blocking experiments showed that monomeric HSA did not bind to this receptor.

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During a 1974 foodborne outbreak of viral hepatitis type A among Navy recruits, we evaluated clinical and laboratory features prospectively in 130 affected persons. The ratio of anicteric to icteric persons identified during the outbreak was 1:3.5 but illness was relatively mild in this population of young adults.

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Five island populations representing the three major cultural groups of the South Pacific--Polynesia, Micronesia, Melanesia--were studied for prevalence of antibody to hepatitis A virus (anti-HAV) and of antibody to the core antigen of hepatitis B virus (anti-HBc). Sera were collected in the late 1950s and early 1960s, selected where possible for appropriate age and sex distributions, and were tested by radioimmunoassay. Rather marked differences in prevalence were observed.

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Two different ultrastructural alterations were observed in liver cells of chimpanzees inoculated with plasma derived from two different patients with non-A, non-B hepatitis. During the acute phase of illness in one group of four chimpanzees, peculiar tubular structures, composed of two unit membranes with electron-opaque material in between, were observed in the cytoplasm of hepatocytes. In contrast, these structures were never detected in the liver cells of the second group of five chimpanzees that received the second inoculum, However, nuclear changes, usually associated with aggregates of 20- to 27-nanometer particles, were found in hepatocytes of the latter animals.

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Twenty-six of 388 patients (6.7%) followed prospectively after open-heart surgery developed non-A, non-B hepatitis. Of these 26, 12 had an elevated (often fluctuating) serum alanine aminotransferase (SGPT) for greater than 1 year.

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Serial serum samples from 22 patients with transfusion-associated non-A, non-B hepatitis and 2 chimpanzees with the experimentally induced disease were tested for circulating immune complexes by Raji-cell radioimmunoassay. 13 patients (59%) and 1 chimpanzee had circulating immune complexes immediately before, coincident with, or during the return to normal of raised aminotransferase activity. 7 of the 10 patients with chronic non-A, non-B hepatitis had detectable complexes at levels which waxed and waned in parallel with changes in serum aminotransferase activity.

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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.

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