Anti-e in primary hepatic carcinoma.
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Biomedical subjects
Publications and source records attributed to B L Murphy.
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A study of the e determinant of hepatitis B surface antigen in an area of hepatitis B hyperendemicity revealed that the presence of e antigen or of antibody to e in the sera of individuals was specifically related to evidence of past or present infection with hepatitis B virus. Among asymptomatic long-term carriers of hepatitis B surface antigen, presence of the e antigen was associated with elevated levels of aspartate and alanine aminotransferases in serum; this observation suggested that the e antigen might be a marker for persisting hepatic dysfunction. Higher levels of DNA polymerase found in carriers of the surface antigen with e antigen suggested that these individuals might have a higher level of circulating Dane particles and thus, perhaps, a higher level of hepatitis B virus infectivity.
Virazole (Ribavirin, ICN 1229), a broad-spectrum, antiviral chemotherapeutic agent was used to treat two adult chronically hepatitis B surface antigen (HB(s) Ag)-seropositive chimpanzees. No significant change in serum hepatitis B surface antigen was noted and no adverse reactions were observed. The role of viral replication in the chronic carrier state of hepatitis B is discussed.
HBc Ag was detected by fluorescent antibody in liver biopsies taken from chronic hepatitis B surface antigen (HBs Ag) carriers having e antigen in their sera. HBc Ag could not be detected in liver biopsies from similar individuals having e antibody in their sera.
Sera of 103 carriers of hepatitis B surface antigen were assayed for e-antigen and anti-e. Twenty-four were e-antigen-positive, 31 anti-e-positive, and 48 had neither detectable (e-negative). Aminotransferases were elevated in 75% of the e-antigen-positive carriers compared with 25% of e-negative carriers (P less than 0.001) and 13% of anti-e-positive carriers (P less than 0.001). Serum DNA polymerase activity was significantly higher in the e-antigen-positive carriers than in carriers without e-antigen. Dane particles were shown in 10 of 12 carriers with e-antigen, compared with one of 12 e-negative carriers (P less than 0.0003) and none of 12 anti-e-positive carriers (P less than 0.00003). These results suggest that ongoing hepatitis B viral replication is more active in e-antigen-positive carriers than in carriers without e-antigen, a finding that may help explain the high prevalence of chronic active hepatitis described in these individuals.
Sera from well individuals, including controls and asymptomatic HBsAg carriers, post-transfusion hepatitis cases, and chronic active liver disease patients were examined for the presence of "e" antigen and e antibody by rheophoresis. Our data confirm the specific association between the e determinant and hepatitis B infections and indicate that e antigen is closely associated with evidence of chronic hepatic dysfunction, in contrast to the association of e antibody with hepatic normalcy in HBsAg carriers. However, these correlations are not absolute and, therefore, it should not be inferred that all e antigen-positive individuals will develop chronic hepatitis nor, conversely, that presence of e antibody invariably protects against the development of chronic hepatitis.
A new antigen/antibody system, "e" and anti-e, was described in 1972. In order to assess the clinical significance of e antigen and anti-e, their presence was correlated with the clinical status, S.G.P.T. levels and liver biopsies of HBsAg carriers. 31 of the carriers had liver biopsies, 32 of 70 carriers had anti-e and 2 had e antigen. 28 of 55 carriers with normal S.G.P.T. and 4 of 15 patients with raised S.G.P.T. had anti-e. This difference is not statistically significant. 2 patients with e had raised S.G.P.T. All patients with normal histology, 45% of patients with mild, and 23% of patients with striking histological changes in the liver had anti-e. This association of anti-e with a normal or mildly abnormal liver was statistically significant. The 2 patients with e antigen had the most severe abnormalities in liver function and liver histology.
We report the temporal patterns of various immunohistological and serological parameters of acute self-limited hepatitis B virus infection of two chimpanzees, and we provide evidence that the synthesis of hepatitis B core antigen precedes that of hepatitis B surface antigen. Our data suggest that existence of a biphasic hepatitis B virus infection involving a hematogenous reinfection of the liver and indicate that recruitment of liver cells to produce hepatitis B virus may occur in a pattern consistent with a replicative cycle of about 8 days.
Transformed chimpanzee lymphocytes were examined to determine whether they would support the replication of hepatitis B virus. After 5 months, no hepatitis B virus, hepatitis B surface antigen, or antibody to hepatitis B surface antigen was detected.
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The ecology of herpesviruses in marmosets and other nonhuman primates is important today, for colonies of these animals are being established for biomedical research. This paper presents the first reported isolations of Herpesvirus tamarinus from throat swabs of a healthy white-lipped marmoset carrier (Saguinus nigricollis) during a 2-month period. Infectivity studies with this virus in both white-moustached (S. mystax) and white-lipped marmosets demonstrated that the virus is not lethal to white-moustached marmosets (perhaps a more resistant species) at 1,000 TCID(50). Which environmental conditions trigger the unmasking of herpesviruses in marmosets is not known. Hoever, intermittent H. tamarinus shedding may help explain spontaneous infections in established colonies as well as suggest an additional mechanism for transmission of virus between marmosets under natural conditions.
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A small, double-stranded deoxyribonucleic acid viral agent (agent Y) has been found in blood from patients with infectious hepatitis. The agent was propagated in chimpanzee liver tissue culture which had been grown and maintained on unheated agamma calf serum. A causal relationship between this agent and the occurrence of human disease cannot be determined from the data presented.
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