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Biomedical subjects

R H Purcell

Publications and source records attributed to R H Purcell.

At least 19 recordsLinked to original sources
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↗
PubMed1979

Circulating immune complexes in non-A, non-B hepatitis. Possible masking of viral antigen.

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. Immune complexes may contain and mask viral antigens, and their presence may explain the failure of conventional immunological techniques to detect virus antigens.

Acute Disease↗
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

Prevalence of antibody to hepatitis A and hepatitis B viruses in selected populations of the South Pacific.

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. Anti-HBc patterns confirmed that HBV is endemic in the Pacific populations. Furthermore, the patterns differed somewhat from each other and did not correlate with ethnogeographic area. Prevalence of anti-HAV was high in all populations studied. A Unique pattern was found for the island of Ponape (Micronesia): In a Ponape population bled in 1963, anti-HAV was not detected in any individual under 20 years of age, but almost all individuals over that age were found to be seropositive. On testing a second group of sera collected in 1975, all individuals aged 14--21 years were found to be antibody positive, indicating that HAV had returned to Ponape sometime prior to 1975. There was no significant difference in the prevalence of HAV or HBV infection between males and females in any of the populations studied.

Adolescent↗
PubMed1979

Sites that bind polymerized albumin on hepatitis B surface antigen particles: detection by radioimmunoassay.

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. In general, the HBsAg particles from sera with HBeAg had more poly-HSA receptor sites or relatively more particles carrying this receptor compared with HBsAg from sera with anti-HBe. Microtiter plates coated with poly-HSA bound HBsAg from sera containing HBeAg with greater efficiency than did anti-HBs coupled to a solid phase (Ausria II beads), whereas with sera positive for anti-HBe, the two assays were equally sensitive. Decreased ability of HBsAg to bind to poly-HSA was seen in some sera which had been stored for a few years at 4 degrees C, whereas the binding to anti-HBs was unaffected. It is possible that polymers of albumin on the surface of hepatocytes could function as receptors for hepatitis B virus.

Animals↗
PubMed1979

Epidemiology and clinical characteristics of acute hepatitis types A, B, and non-A non-B.

A consecutive series of 115 patients hospitalized with acute viral hepatitis in Copenhagen was studied for serological markers for hepatitis A and B virus. Thirty-nine patients had type B, 66 had type A, 3 had both type A and B, and 7 had type non-A non-B. Of the patients 81% were between 15 and 40 years of age, and there was a dominance of males due to an overrepresentation of homosexual males (30%) in both the A and B group. The main type of exposure to hepatitis type A was travel to foreign countries (53%), and for type B it was drug addiction (41%). In types A and B the duration of jaundice was positively correlated to the age of the patients but did not vary with sex or type of exposure. There was no difference in maximum alanine aminotransferase levels between the groups, but maximum bilirubin levels were lower for the type A group. Patients with hepatitis type A had a higher level of IgM than those with type B and with type non-A and non-B. We conclude that both clinically acute hepatitis type A and type B occur mainly in young adults and that foreign travel, drug addiction, and homosexuality increase the risk of getting acute hepatitis.

Acute Disease↗
PubMed1979

The chronic sequelae of non-A, non-B hepatitis.

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. Liver biopsy, done in eight of 12, showed chronic active hepatitis in six and chronic persistent hepatitis in two; one patient with chronic active hepatitis had early cirrhosis. Anicteric patients with peak SGPT greater then 300 IU/L were at greatest risk of developing chronic hepatitis. Chronic non-A, non-B hepatitis was symptomatically mild and unaccompanied by physical signs or laboratory evidence of autoimmune disease or severe chronic liver disease. In all 12 patients there was spontaneous improvement in serum transaminase over a period of 1 to 3 years, and four patients had sustained normalization of SGPT. Thus chronic active hepatitis is a common sequela of acute non-A, non-B hepatitis but may have a better prognosis than chronic active hepatitis of other causes.

Acute Disease↗
PubMed1978

Anti-HBc, HBeAg and DNApolymerase activity in healthy HBsAg carriers and patients with inflammatory liver diseases.

In this paper we report on anti-HBc-titers, HBcAg, DNApolymerase activity in the serum and intracellular HBsAg in healthy HBsAg-carriers and patients with HBsAg-positive inflammatory liver diseases. 32/44 patients with acure virus-B-hepatitis were negative for anti-HBc in the first week of the disease. Anti-HBc-titers in healthy HBsAg-carriers varied between 1:10 and 1:32,000 (medium titer 1:4,000). In HBsAg-positive CAH we found a medium titer between 1:32,000 and 1:64,000, in cases with CPH of about 1:16,000. All autoimmune type CAH showed anti-HBc-titers less than 1:10. By immunofluorescence we could demonstrate in a group of 71 asymptomatic HBsAg-carriers in none of the healthy HBsAg-carriers HBcAg in the liver cell nuclei. In contrast HBcAg could only be found in 4/5 HBsAg positive CAH- and 6/9 CPH patients. No elevated DNApolymerase activity could be demonstrated in healthy HBsAg-carriers. Out of 44 patients with virus-B-hepatitis only 3 showed elevated DNApolymerase activity. On the other hand DNApolymerase elevation was demonstrable in 17/37 cases with CAH and 9/15 with CPH. The investigations showed a strong correlation between the demonstration of HBcAg in the serum and the DNApolymerase activity. The characteristic findings enabled us to differentiate between "healthy" HBsAg-carriers and HBsAg-carriers with inflammatory liver diseases.

Alanine Transaminase↗
PubMed1978

Transmissible agent in non-A, non-B hepatitis.

Plasma or serum from 4 patients with acute or chronic non-A, non-B post-transfusion hepatitis (P.T.H.) and from a blood-donor implicated in two cases of P.T.H. was inoculated into 5 chimpanzees. Biochemical and histological evidence of hepatitis developed in these 5 chimpanzees but not in a control animal. The mean incubation period in the chimpanzees was 13.4 weeks, compared with 7.7 weeks in the 4 patients with P.T.H. The peak alanine aminotransferase (A.L.T.) levels in the 5 chimpanzees were 265, 212, 219, 70, and 62 I.U./l. Histological changes ranged from mild to conspicuous hepatitis and generally correlated with the degree of A.L.T. elevation. There was no evidence of clinical disease and all animals went on to biochemical and histological recovery. There was no serological evidence of type A or type B hepatitis. Hepatitis was transmitted by serum derived from patients with chronic as well as acute hepatitis, strongly suggesting a chronic carrier state for the agent responsible for non-A, non-B hepatitis. Non-A, non-B hepatitis thus seems to be due to a transmissible agent which can persist and remain infectious for long periods.

Acute Disease↗
PubMed1978

Spontaneous resolution of severe aplastic anemia associated with viral hepatitis A in a 6-year-old child.

Recovery from acquired aplastic anemia associated with hepatitis is rare. This case of a 6-year-old boy with severe aplastic anemia is the first reported association of this disease with a hepatitis A infection. Antibody to hepatitis A (anti-HA) was not detected on admission, but was detected three weeks later. Infection with hepatitis B virus, cytomegalovirus (CMV), and Epstein-Barr virus (EBV) were excluded. The peak titer of anti-HA was higher than would be expected for passive transfer of antibody resulting from transfusions. The persistence of antibody for more than 20 months after the last transfusion was not consistent with passive antibody, which would be expected to disappear over that time. This child had indications for allogeneic marrow transplant and a sibling donor who was histocompatible. However, the transplant was postponed because the prognosis was considered to be poor in the presence of active hepatitis. There was a spontaneous remission without the necessity of the transplantation procedure.

Anemia, Aplastic↗
PubMed1978

The viral hepatitides.

Vaccines and chemotherapy may soon strengthen the armamentarium for control of type B hepatitis. The incidence of type A is still declining in the U.S., and now that type non-A, non-B has been transmitted to animals, a marker for it is being widely sought.

Animals↗
PubMed1978

Hepatitis A virus infection: new insights from seroepidemiologic studies.

The prevalence of exposure to hepatitis A virus (HAV) increases with increasing age; decreases with increasing socioeconomic class; increases with increasing serologic evidence of prior hepatitis B virus (HBV) exposure but is much more common than HBV exposure; is independent of sex and race; varies in different parts of the world as a function of hygienic, developmental, and unrecognized geographic factors; and is not affected by immune deficiency or immaturity. Transmission of type A hepatitis is enhanced by poor personal hygiene such as that seen in institutions for the mentally retarded. On the other hand, there is no increased exposure to HAV among homosexuals, who have frequent and intimate contact with multiple sexual partners; among hemodialysis patients and staff; or among multiply transfused individuals, all of whom are at significantly increased risk of exposure to HBV. No epidemiologic evidence has confirmed the existence of viremic or intestinal carriers of HAV, and the virus is rarely, if ever, spread by parenteral mechanisms. Finally, HAV appears to play no role in chronic liver disease and a very minor role in fulminant hepatitis; however, HAV is responsible for a sizable proportion (approximately 20%--40%) of sporadic hepatitis among urban adults.

Age Factors↗
PubMed1978

Localization of hepatitis A antigen in marmoset organs during acute infection with hepatitis A virus.

Twelve marmosets (Saguinus mystax) were inoculated intravenously (iv) with hepatitis A virus (HAV). One died early (day 12); seven were sacrificed at the time of elevation in level of alanine aminotransferase (serum glutamic-pyruvic transaminase), and four without elevation were not sacrificed but seroconverted. In the seven marmosets sacrificed during the acute stage of illness, hepatitis A antigen (HA Ag) was detected in the liver by immunofluorescence in all cases, by immune electron microscopy in four, and by enzyme-linked immunosorbent assay (ELISA) in three. The HA Ag appeared by immunofluorescence as very fine granules in the cytoplasm of hepatocytes and Kupffer cells. The HA Ag could not be detected by immunofluorescence in biopsy specimens taken from the duodenum, jejunum, ileum, or transverse colon in any of eight marmosets in which necropsy was performed during the acute or preacute stage of illness. These findings suggest that the gut is not involved during the acute phase of HAV infection following iv inoculation into marmosets. The ELISA results showed that only three of 12 marmoset livers obtained during the acute phase of HAV infection could be used as an antigen source in serologic testing for antibody to HA Ag. Thus, marmoset livers were no better as a source of HA Ag than acute-phase stools from patients with type A hepatitis.

Acute Disease↗