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Biomedical subjects

R H Purcell

Publications and source records attributed to R H Purcell.

At least 289 records · Page 16Linked to original sources
PubMed1980

Epidemic and endemic hepatitis in India: evidence for a non-A, non-B hepatitis virus aetiology.

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. A large proportion of hepatitis in India seems to be caused by previously unrecognised agents.

Adolescent↗
PubMed1980

Epidemiology of HBV-associated delta agent: geographical distribution of anti-delta and prevalence in polytransfused HBsAg carriers.

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.S.A. In view of the failure to detect delta in the absence of markers of HBV, the prevalence of anti-delta among polytransfused HBsAg carriers suggests that the delta-associated agent is transmitted by superinfection or coinfection of HBsAg carriers, the HBsAg carrier state possibly providing a rescue function to the superinfecting agent.

Carrier State↗
PubMed1980

Detection of antibodies to single-stranded DNA in naturally acquired and experimentally induced viral hepatitis.

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). No consistent pattern was observed with either technique, indicating the elevated levels of this antibody are not as reliable markers of parenchymal liver damage as had been previously suggested.

Animals↗
PubMed1980

delta Agent: association of delta antigen with hepatitis B surface antigen and RNA in serum of delta-infected chimpanzees.

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 1.24-1.25 g/cm3 and sedimented with a mobility intermediate between that of the hepatitis B virion and that of the 22-nm form of HBsAg. The particles contained only indistinct internal structure by electron microscopy and were not unique to delta agent infection, similar particles without delta-antigen activity being observed in the preinfection serum of HBsAg carrier chimpanzees. A small RNA (Mr, 5 X 10(5)) was temporally associated with delta antigen in the serum of infected chimpanzees and copurified with the delta-antigen-associated particles. This RNA is smaller than the genomes of known RNA viruses but larger than the viroids of higher plants.

Animals↗
PubMed1980

Transmission of the hepatitis B virus-associated delta antigen to chimpanzees.

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. In chimpanzees with circulating HBsAg at the time of inoculation, synthesis of delta occurred earlier and its extent and duration were greater than in animals previously unexposed to HBV; coincident with synthesis of delta, hepatitis occurred in chronic HBsAg carriers, and synthesis of preexisting HBV gene products (HBsAg and hepatitis B core antigen) was diminished. Delta appears to be a marker of a transmissible pathogenic agent, either an HBV variant or another agent that requires the helper functions of HBV, that is defective and interferes with HBV replication.

Animals↗
PubMed1980

Hepatitis A virus in the liver and intestine of marmosets after oral inoculation.

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. None of the remaining marmosets sacrificed from days -3 to 31 survived long enough to develop antibody to HAV, but an additional two marmosets, which were sacrificed on days 21 and 31, demonstrated HAV in their livers and also in bile but not in the intestinal tissues or their contents. The mesenteric lymph nodes and spleens were negative for HAV by immunofluorescence in all the marmosets. No evidence of HAV replication was demonstrated in any part of the intestine at any time during the incubation period or during acute illness in the marmosets inoculated orally with HAV. The shedding of HAV in stools in the late incubation period can be explained by excretion of HAV from the livers with the bile.

Alanine Transaminase↗
PubMed1980

PLC/PRF/5 (Alexander) hepatoma cell line: further characterization and studies of infectivity.

The Alexander hepatoma cell line, PLC/PRF/5, was studied for evidence of hepatitis B virus markers and alpha-fetoprotein. Only hepatitis B surface antigen and alpha-fetoprotein were detected. Induction experiments with 5-iodo-2'-deoxyuridine and inoculation of chimpanzees with whole cells or tissue culture fluid did not reveal evidence of synthesis of additional hepatitis B virus markers or of production of infectious virus.

Animals↗
PubMed1980

Etiological characterization of hepatitis B surface antigen-negative hepatitis among adult patients in Athens, Greece.

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. A total of 7 of the 19 patients had serological evidence of hepatitis A virus infection, and 2 had evidence of recent hepatitis B virus infection. The remaining 10 patients lacked evidence of hepatitis A virus, hepatitis B virus, cytomegalovirus, or Epstein-Barr virus infection related to their illness and were classified as having type non-A, non-B hepatitis. Types A and non-A, non-B hepatitis were clinically similar in these adults patients. However, patients with type non-a, non-B hepatitis were, on the average, older and more likely to have received parenteral inoculations during the 6 months before contracting hepatitis. Approximately 76% of the 216 consecutive cases of acute viral hepatitis were probably type B, approximately 10% were probably type A, and approximately 14% were probably type non-A, non-B, although the latter two types may be underestimated because of the possibility of superinfection with these viruses in asymptomatic hepatitis B surface antigen carriers. Thus, all three types of viral hepatitis appear to be important in the etiology of liver disease in Athens, Greece.

Acute Disease↗
PubMed1980

Hepatitis type A, B, and non-A non-B in fulminant hepatitis.

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. Two of these had been treated with disulfiram and a drug aetiology could not be excluded, but in six patients no known cause of fulminant hepatitis could be determined and these patients were classified as having hepatitis type non-A non-B. The survival rate was not statistically different for patients having type A, B, or non-A non-B hepatitis.

Acute Disease↗
PubMed1980

The role of acute hepatitis type A, B, and non-A non-B in the development of chronic active liver disease.

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. None had serological markers of actual hepatitis type A infection. Of the 74 patients with a histologically complete resolution, the acute episode could be classified as type B hepatitis in 47 and type A hepatitis in 13 patients. The remaining 14 patients were classified as having acute viral hepatitis type non-A non-B. Our findings confirm that type B and non-A non-B hepatitis may give rise to chronic liver disease, whereas type A hepatitis so far has not been demonstrated to initiate a chronic liver disease.

Age Factors↗
PubMed1979

Incidence and significance of antibodies to delta antigen in hepatitis B virus infection.

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 19.1% and 2.6% of sera from patients with chronic hepatitis and symptomatic chronic carriers, respectively, and was not detected in the sera of HBsAg-negative controls. Anti-delta antibody appeared transiently and in low titres (less than 1:500) in 4.8% of sera from patients with acute type B hepatitis. The presence and persistence of anti-delta antibody seem to be associated with chronic HBV infection and the development of progressive liver damage.

Acute Disease↗
PubMed1979

Non-A, non-B hepatitis: ultrastructural evidence for two agents in experimentally infected chimpanzees.

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. Although these particles resembled viruses, they were not as uniform as small virus particles often appear. In five other chimpanzees inoculated with non-A, non-B hepatitis material not known to be related to the first two inocula, cytoplasmic structures were found in four, and nuclear structures were found in the remaining one. Thus, all 14 chimpanzees inoculated with transmissible non-A, non-B hepatitis agents could be classified as having either nuclear or cytoplasmic changes. These observations add support to epidemiologic data suggesting that there may be more than one agent of non-A, non-B hepatitis.

Animals↗