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Biomedical subjects

R H Purcell

Publications and source records attributed to R H Purcell.

At least 37 records · Page 2Linked to original sources
PubMed1978

Antigens of hepatitis B virus: failure to detect HBeAg on the surfaces of HBsAg forms.

The particulate forms of HBsAg were analysed for the presence of HBeAG on their surfaces. By immunodiffusion analysis, anti-HBe did not form precipitin bands with the purified forms of HBSAg and hyperimmune guinea pig antisera to these forms did not react with HBeAg. Lines of non-identity were observed between the HBeAg determinants (e1 and e2) and the Dane particles and filaments isolated from an HBeAg-positive serum. Finally, anti-HBe failed to precipitate the polymerase-positive subpopulation of Dane particles, indicating that anti-HBe has no direct role in virus neutralization.

Animals↗
PubMed1978

Urethral infection of chimpanzees by Ureaplasma urealyticum.

Two strains of Ureaplasma urealyticum serotype V that had produced urethritis in human volunteers were, after a number of subcultures in artificial media, introduced intra-urethrally into three chimpanzees. One strain given to two chimpanzees rapidly multiplied 1000-fold whereas there was less evidence that organisms of another strain multiplied in a third animal. Over a 14-day period the ureaplasmas persisted in all animals, did not spread to the throat and did not produce an inflammatory response. After this time they were eliminated by tetracycline therapy.

Animals↗
PubMed1978

Enzyme-linked immunosorbent assay for detection of hepatitis A antigen in stool and antibody to hepatitis A antigen in sera: comparison with solid-phase radioimmunoassay, immune electron microscopy, and immune adherence hemagglutination assay.

Previously described techniques for detection of hepatitis A antigen (HA Ag) and antibody (anti-HA) have required purified HA Ag and expensive equipment. Herein is described an enzyme-linked immunosorbent assay (ELISA) for specific detection of HA Ag in human stool filtrates and of anti-HA in sera by using selected HA Ag-containing human stool filtrates as the antigen source. Because human stools often react nonspecifically in serological tests for HA Ag, blocking with preexposure and hyperimmune anti-HA sera from a chimpanzee inoculated with hepatitis A virus was used to confirm specific detection of HA Ag. The sensitivity of ELISA was found to be comparable to that of solid-phase radioimmunoassay (SPRIA) and immune electron microscopy (IEM). Of 37 acute-phase stools collected from nine patients, 16 were positive for HA Ag by ELISA. In 13 of these, HA Ag particles were found by IEM, and an additional 3 stools negative by ELISA contained HA Ag particles by IEM. Eight control stools were negative by both ELISA and IEM. Anti-HA was measured in sera by demonstrating its ability to block binding of the enzyme conjugate to HA Ag in a stool without detectable nonspecificity. This test (blocking ELISA) was as sensitive and specific as blocking SPIRA, IEM, and immune adherence hemagglutination and, like SPRIA and IEM, detected early-developing antibody. The ELISA is simple to perform and requires only a minimum of equipment. It is useful for screening stools for HA Ag and for monitoring HA Ag during purification, as well as for detecting early and late anti-HA in sera.

Acute Disease↗
PubMed1978

Type B hepatitis after needle-stick exposure: prevention with hepatitis B immune globulin. Final report of the Veterans Administration Cooperative Study.

Hepatitis B immune globulin (HBIG) and immune serum globulin (ISG) were examined in a randomized, double-blind trial to assess their relative efficacies in preventing type B hepatitis after needle-stick exposure to hepatitis B surface antigen (HBsAG)-positive donors. Clinical hepatitis developed in 1.4% of HBIG and in 5.9% of ISG recipients (P = 0.016), and seroconversion (anti-HBs) occurred in 5.6% and 20.7% of them respectively (P less than 0.001). Mild and transient side-effects were noted in 3.0% of ISG and in 3.2% of HBIG recipients. Available donor sera were examined for DNA polymerase (DNAP) and e antigen and antibody (HBeAg; anti-HBE). Both DNAP and HBeAg showed a highly statistically significant correlation with the infectivity of HBsAg-positive donors. Hepatitis B immune globulin remained significantly superior to ISG in preventing type B hepatitis even when the analysis was confined to these two high-risk subgroups. The efficacy of ISG in preventing type B hepatitis cannot be ascertained because a true placebo group was not included.

Adolescent↗
PubMed1978

Localization of hepatitis A antigen in liver tissue by peroxidase-conjugated antibody method: light and electron microscopic studies.

Hepatitis A antigen (HAAG) was localized in liver tissue from marmosets inoculated with human hepatitis A virus (HAV) by light and electron microscopy by using a peroxidase-conjugated antibody method. The fine granular peroxidase staining was scattered throughout the cytoplasm of liver cells when viewed with the light microscope. The distribution of HAAg-positive cells was focal. Virus-like particles, 24 to 27 nm in diameter, were observed in the cytoplasm of hepatocytes and smaller cells, resembling Kupffer cells, by standard thin-section electron microscopy (thin section EM). By immunoperoxidase electron microscopy (immunoperoxidase EM), HAAg was detected on the particles, which were aggregated within cytoplasmic vesicles of the hepatocyte. The surrounding membrane of the vesicles was also HAAg- positive. Similar HAAg particles were observed in the cytoplasm of smaller cells adjacent to hepatocytes as well. Thus, immunoperoxidase EM revealed that the 24- to 27-nm virus-like particles in the cytoplasm of liver cells obtained from marmosets were infected with HAV contained HAAg.

Animals↗
PubMed1978

Anti-HBc titers in HBeAg and anti-HBe positive asymptomatic HBsAg carriers.

A study was undertaken to establish markers for HBV replication in relation to HBeAg and anti-HBe. HBsAg carriers with serum HBeAg had DNA polymerase activity in the serum and HBcAg in the liver nuclei. Anti-HBe positive and anti-HBe/HBeAg negative sera lacked these markers. For anti-HBc the following geometrical mean titers were calculated: 1: 12,000 for HBeAg positive, 1:9, 100 for anti-HBe and anti-HBc positive, and 1:2,800 for anti-HBc positive anti-HBe/HBeAg negative asymptomatic HBsAg carriers. Follow up studies revealed mostly unchanged anti-HBc titers in all three groups over an observation period of ten to twenty months. Our data argue for a prolonged HBV replication in all HBsAg carrier subgroups compared to individuals with an uncomplicated acute virus-B-hepatitis. This study gives no final answer whether HBeAg negative HBsAg carriers have a continous HBV replication.

Antibodies, Viral↗
PubMed1978

Hepatitis B vaccines. On the threshold.

Experimental hepatitis B vaccines have recently been developed and are undergoing preliminary evaluation. These vaccines are unique in that they are prepared from viral antigen purified from the plasmas of human chronic carriers because hepatitis B virus has not been cultivated in vitro. They appear to be safe and antigenic, but care must be exercised in their evaluation because of the potential risks inherent in all vaccines.

Animals↗
PubMed1977

Antibody to hepatitis A antigen in institutionalized mentally retarded patients.

Institutionalized patients with Down syndrome and matched controls with other causes of mental retardation were tested by immune adherence hemagglutination for the presence of antibody to hepatitis A antigen (anti-HA). Altogether 75.1% (175 of 233) exhibited presence of anti-HA, with no differences by sex or age. Patients reactive for hepatitis B surface antigen (HBsAg) or its antibody (anti-HBs) were reactive for anti-HA significantly more frequently than those with a negative reaction for these markers. In contrast to serologic markers of hepatitis type B, prevalence of anti-HA does not depend on the cause of mental retardation or on the age at primary infection. The rate of anti-HA positivity was found to be closely correlated with duration of institutionalization. The study confirmed that many closed institutions for the mentally retarded are hyperendemic for hepatitis type A and that formation of anti-HA is not greatly affected by either immune deficiency or immune immaturity.

Adolescent↗
PubMed1977

Non-B hepatitis in Melbourne: a serological study of hepatitis A virus infection.

A study was performed to establish the value of immune adherence haemagglutination tests for antibody to hepatitis A virus in the diagnosis of non-B hepatitis. Infection with hepatitis A virus was confirmed in 14 out of 16 patients from six families and seven out of nine patients in whom the source of infection was unknown. One additional patient, who had had two episodes of jaundice, was shown to have had an attack of hepatitis A followed by an attack of hepatitis B. In patients with acute hepatitis A antibody detectable by immune adherence haemagglutination becomes detectable three or four weeks after the onset of symptoms and reaches peak levels about five weeks later.

Adolescent↗
PubMed1977

Multiple hepatitis viruses in multiple attacks of acute viral hepatitis.

We evaluated the causes of 30 episodes of acute viral hepatitis in 13 patients who had multiple attacks. Two (seven per cent) of 30 bouts were caused by hepatitis A virus, and 12 (40%) by hepatitis B virus. No patient, however, had more than one attack with the serologic characteristics of Type A or Type B disease. Thus, there were 16 bouts (53 per cent) not attributable to either of the two recognized hepatitis viruses. None of these "non-A, non-B" episodes, evaluated for infectious mononucleosis and cytomegalovirus infection, could be ascribed to either. From this evidence, therefore, it appears that the clinical syndrome of viral hepatitis is produced not only by the two viruses (hepatitis A virus and hepatitis B virus) recognized since the 1940's but also, in all probability, by two non-A, non-B agents.

Acute Disease↗