T lymphocyte subsets in parenteral and non-parenteral heroin abusers in Britain.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
H C Thomas
Publications and source records attributed to H C Thomas.
The role of delta superinfection in acute exacerbations of chronic type B hepatitis.
Serum specimens collected from patients with chronic type B hepatitis during their acute exacerbations were studied with radioimmunoassay for serological markers of delta (delta) agent infection. Serum delta antigen was negative in all 56 hepatitis B e antigen (HBeAg)-positive and 25 anti-HBe-positive acute exacerbations. Two (3.6%) HBeAg-positive and five (20%) anti-HBe-positive acute exacerbations were found to be positive for both IgG anti-delta and IgM anti-delta. The incidence in anti-HBe-positive patients was significantly higher than in HBeAg-positive patients. These results indicated that some of the acute exacerbations, particularly in anti-HBe-positive phase, could be attributed to delta-superinfection. However, acute exacerbations preceding HBeAg/anti-HBe seroconversion were not associated with delta-superinfection.
Hepatitis Antibodies↗
Relationship of HLA protein display to activation of 2-5A synthetase in HBe antigen or anti-HBe positive chronic HBV infection.
In this study we have examined the density of HLA class I protein display on the hepatocytes of patients with HBe antigen (HBeAg) or anti-HBe (HBeAb) positive chronic hepatitis B virus (HBV) infection and related this to the level of interferon activation of these cells determined by measuring hepatic oligo 2-5A synthetase activity. In HBeAg positive patients the density of HLA class I (HLA-I) protein was not significantly increased above that found in uninfected liver, but levels of 2-5A synthetase were twice normal. In anti-HBe positive patients, HLA-I density was markedly increased in the presence of normal 2-5A synthetase activity. These data are consistent with type I (alpha or beta) interferon activation of the hepatocytes in HBeAg positive patients and type II (gamma) interferon activity in anti-HBe positive subjects.
2',5'-Oligoadenylate Synthetase↗
Has immunology become important to hepatologists?
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Antibody Formation↗
Cheaper immunisation against hepatitis B.
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Hepatitis B↗
Treatment of chronic hepatitis due to hepatitis B virus.
A clearer view of the natural history of chronic hepatitis B virus (HBV) infection has permitted recognition of a phase of viral replication associated with progressive liver damage, and one of absent replication when the disease is inactive and when continued presence of hepatitis B surface antigen (HBs) is due to the integration of viral genes with the host genome. These two phases can be identified by HBe antigenaemia and anti-HBe, respectively. Several active antiviral drugs are available and may significantly benefit certain HBe Ag-positive groups. The antiviral activity of vidarabine and its analogues and of alpha-interferons is established, and insight is being gained into factors that predict response. In general, results depend on duration of infection, and integrity of the patient's immune response. Anti-HBe positive carriers usually need no treatment, but in those with continuing low-level HBV replication or delta superinfection antiviral therapy, although of unproven value, may be tried. In patients without HBV or hepatitis delta virus (HDV) replication who have signs of active disease, immunosuppressants may be tried with benefit.
Acyclovir↗
Hepatitis B virus DNA in saliva, urine, and seminal fluid of carriers of hepatitis B e antigen.
Concentrated samples of saliva, urine, and seminal fluid from 23 men with chronic liver disease who were positive for hepatitis B e antigen were examined for the presence of hepatitis B virus deoxyribonucleic acid (HBV-DNA) by molecular hybridisation. HBV-DNA was detected in saliva from 15 of 17 men (88%), urine from 12 of 22 men (55%), and seminal fluid from 13 of 21 men (62%). The presence of hepatitis B virus in such secretions has important epidemiological implications for heterosexual and homosexual contact.
Autoradiography↗
Expression of beta-2-microglobulin on hepatocytes after liver transplantation.
The distribution of beta 2-microglobulin was studied by an immunoperoxidase method in paraffin sections from sixteen serial graft liver biopsy samples taken after liver transplantation from four patients who had received transplants for advanced primary biliary cirrhosis. Mild to moderate acute rejection was diagnosed in three of the patients. Expression of beta 2-microglobulin on hepatocyte membranes was greater during rejection, and tended to fall after the rejection episode. However, a few hepatocytes continued to display beta 2-microglobulin on their cell membranes. Rejection was characterised histologically by infiltration of portal tracts with lymphoid cells, and cholestasis. Enhanced display of beta 2-microglobulin on hepatocytes probably reflects display of HLA A, B, and C antigens and may be associated with increased susceptibility of the affected cells to T-lymphocyte-mediated immune attack.
Biopsy↗
Non-A, non-B hepatitis after intravenous gammaglobulin.
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Alanine Transaminase↗
Clinical evaluation of a monoclonal assay for hepatitis B surface antigen: identification of "HBsAg-like" polypeptides non-reactive in conventional radioimmunoassays.
An immunoradiometric assay for hepatitis B surface antigen (HBsAg) that employs monoclonal antibodies directed against the common epitope(s) of HBsAg was used to analyse 3,694 samples of human serum. Further analysis of those sera identified as HBsAg-positive in this assay demonstrated that the findings with the monoclonal-antibody-based assay correlated with the presence of HBsAg as determined by Austria II. A small proportion of apparently false-positive reactions were observed, in that some sera, although reactive with the monoclonal antibodies, were not positive in conventional immunoassays using polyclonal antisera, nor were they neutralisable with polyclonal anti-HBs. The material purified by monoclonal immunoabsorbants from representative "true" and "false-positive" sera was run on polyacrylamide gels and examined under the electron microscope. The antigen in the apparently false-positive sera contained some polypeptides of similar size to those found in HBsAg, but no virus particles were seen by electron microscopy. The majority of patients with this monoclonal-antibody-reactive antigen gave either a history of hepatitis B virus (HBV) contact or had signs of liver disease.
Antibodies, Monoclonal↗
Hepatitis D virus antibody in HBsAg-positive and HBsAg-negative substance abusers with chronic liver disease.
The hepatitis D virus (HDV; previously called the "delta agent") is a defective organism which can replicate only in the presence of the hepatitis B virus (HBV). We tested the serum of 95 substance abusers, all of whom had sufficient evidence of chronic liver disease to warrant a liver biopsy, for hepatitis D virus antibody (anti-HDV). Anti-HDV was detected in five of eight hepatitis B surface antigen (HBsAg)-positive patients and 12 of 87 (14%) HBsAg-negative patients. Antibody to the hepatitis B core antigen (anti-HBc) was the sole hepatitis B marker in eight of the 12 (67%) anti-HDV-positive, HBsAg-negative patients but in only 14 of 75 (19%) anti-HDV-negative, HBsAg-negative patients (P less than 0.005). None of the anti-HDV-positive, HBsAg-negative patients had detectable IgM anti-HBc in the serum or hepatitis D antigen in liver tissue, and they had similar clinical features and liver biopsy diagnoses to HBsAg-negative patients without anti-HDV. We conclude that anti-HDV in HBsAg-negative substance abusers reflects infection with HDV and HBV in the distant past and does not indicate more severe liver disease than that seen in HBsAg-negative patients without anti-HDV.
Adult↗
Neutralization of hepatitis B virus infectivity by a murine monoclonal antibody: an experimental study in the chimpanzee.
Two study chimpanzees were inoculated intravenously with approximately 1,000 chimpanzee infectious doses of hepatitis B virus (HBV), one with subtype adr and one with subtype ayw, each previously incubated with 0.1 ml of a murine monoclonal antibody (IgG 1(K) class) directed against a single epitope on hepatitis B surface antigen common to most or all HBV. Two control chimpanzees received identical doses of HBV not incubated with the murine anti-HBs. Neither study chimpanzee developed HBV infection during 12 months of follow-up as judged by normal serum aminotransferase activity, normal liver biopsies, and negative serological tests for HBV-associated antigens and antibodies. In contrast, both control chimpanzees became infected by HBV as evidenced by elevated serum aminotransferase activity, liver biopsy changes characteristic of viral hepatitis, and the appearance of hepatitis B surface antigen (HBsAg) in their sera. Both study chimpanzees were shown to be fully susceptible to infection with these same HBV inocula when challenged 15 months after the initial inoculations at a time when passively administered anti-HBs was no longer detectable. Prior to challenge with HBV, one of the two study chimpanzees received a second injection of the same volume of the murine monoclonal anti-HBs. The survival of this anti-HBs in serum was reduced from six weeks (after the initial injection) to approximately two weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Protection against hepatitis B virus infection by immunization with hepatitis B core antigen.
Although antibody to the hepatitis B surface antigen usually provides protection against hepatitis B virus (HBV) infection, recent reports indicate that this is not always the case. To study the possible role of immune responses to hepatitis B core antigen in immunity to HBV infection, chimpanzees were immunized with chimpanzee liver-derived or genetically cloned hepatitis B core antigen and later challenged with known infectious HBV. Two chimpanzees, which received liver-derived or cloned hepatitis B core antigen in Freund's adjuvant and developed hepatitis B core antibody and low-titer hepatitis B e antibody, were completely protected against HBV infection following challenge. In contrast, another chimpanzee, which received liver-derived hepatitis B core antigen without adjuvant, developed hepatitis B core antibody only in serum and had a subclinical HBV infection when challenged. These findings demonstrate that protection against HBV infection can be induced by immunization with hepatitis B core antigen in adjuvant and that protection, in this case, is not solely dependent on hepatitis B surface antibody. This fact has important implications in our understanding of the biology of HBV infection and in the design of future hepatitis B vaccines.
Animals↗
Clinical uses of HBV-DNA assays.
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DNA, Viral↗
Studies of HBV replication during acute hepatitis followed by recovery and acute hepatitis progressing to chronic disease.
The serologic and viral profiles of 24 patients who presented with acute hepatitis B virus (HBV) infection were studied. Although in rare cases, HBV-DNA was detectable before hepatitis B surface antigen (HBsAg) and e antigen (HBeAg), in the majority the viral proteins appeared first. In acute hepatitis followed by recovery, as IgM anti-HBc (hepatitis B core antigen) titres rose, the level of HBV replication fell and serum transaminases became elevated. In patients progressing to chronic HBV infection, IgM anti-HBc titres rose early, viral replication was initially low but continued to rise as the serum transaminase levels became elevated. 7S IgM anti-HBc, although present in the phase of established chronic HBV infection, was not found in the early phase of the chronic infection. Thus this antibody appears to be a consequence of, rather than a causative factor in, chronic HBV infection.
DNA, Viral↗
Diminished responsiveness of homosexual men to antiviral therapy for HBsAg-positive chronic liver disease.
To identify factors predicting response to antiviral therapy, we reviewed the clinical features of 38 male hepatitis B surface antigen (HBsAg) carriers who received adenine arabinoside or lymphoblastoid interferon. All patients were followed for one year or longer. Response was defined as loss of hepatitis B e antigen, hepatitis B virus DNA and DNA polymerase from the serum. Only 2 of 19 (11%) homosexual men responded, compared with 10 of 19 (53%) heterosexual men (P less than 0.02). Both responders in the homosexual group had received lymphoblastoid interferon. None of the 13 homosexual men, but 8 of 16 heterosexual men, responded to adenine arabinoside or its monophosphate (P less than 0.01). Responders to antiviral therapy had higher (P less than 0.05) serum levels of aspartate aminotransferase (median 115, range 51-344) than did non-responders (median 83, range 32-181). The decreased responsiveness of homosexual men to antiviral therapy may be a result of more severe immunologic abnormalities in homosexual than in heterosexual men with HBsAg-positive chronic liver disease.
Adult↗
Detection of serum HBV-DNA by molecular hybridisation. Correlation with HBeAg/anti-HBe status, racial origin, liver histology and hepatocellular carcinoma.
The relationship of the presence of hepatitis B virus (HBV) DNA in serum, a measure of HBV-replication, to HBeAg/anti-HBe status has been examined. In Northern Europe, there is a strong positive correlation between the presence of HBV-DNA and HBe antigenaemia and a negative correlation with the presence of anti-HBe. These associations are less marked in patients from Southern Europe, Africa, the Middle and Far East. When HBV-DNA is present in the serum of anti-HBe carriers, it is usually associated with the presence of severe liver disease or carcinoma. Forty percent of patients with hepatocellular carcinoma had evidence of continuing HBV replication.
Carcinoma, Hepatocellular↗