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At least 19 recordsLinked to original sources
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↗
PubMed1979

Non-B hepatitis in Japanese recipients of blood transfusions: clinical and serologic studies after the introduction of laboratory screening of donor blood for hepatitis B surface antigen.

Cases of hepatitis virus infection in Japanese recipients of blood transfusions were serologically and clinically analyzed after the introduction of laboratory screening of donor blood for hepatitis B surface antigen by counter immunoelectrophoresis. Non-A, non-B hepatitis occurred in 116 (10.7%) and hepatitis type B in nine (0.9%) of the 1,082 recipients. The incubation period of the post-transfusion non-A, non-B hepatitis cases varied from two to 33 weeks, but most occurred within 15 weeks. In 97 (83.6%) of the 116 cases of non-A, non-B hepatitis studied, the duration of abnormal elevation of the level of serum alanine aminotransferase (glutamic-pyruvic transaminase [SGPT]) was 16 weeks. The cases of non-A, non-B hepatitis could be divided into three groups according to the pattern of elevation of SGPT levels. These findings may suggest either a multiple etiology for non-A, non-B hepatitis or a variety of clinical symptoms with a single etiology for the infection.

Alanine Transaminase↗
PubMed1975

Hepatitis B immune globulin as a prophylactic measure for spouses exposed to acute type B hepatitis.

Because the value of usual immune globulin preparations in preventing Type B hepatitis is doubtful, we carried out a double-blind comparison of a control human immune globulin preparation with one--identified as HBIG--that had a high concentration (442 mug per milliliter) of antibodies to surface components of hepatitis B virus. Effectiveness was tested in spouses of patients with acute Type B hepatitis. Within 150 days after injection, nine of 33 spouses in the control group had symptomatic Type B hepatitis, compared with one of 25 spouses receiving HBIG. One non-B case also occurred in the HBIG group. Five control globulin recipients had evidence of subclinical hepatitis B infection, compared with one HBIG recipient. Thus, HBIG appeared effective in suppressing not only disease, but also infection itself. Prophylactic value has been demonstrated in persons who should now be recognized as being at exceptionally high risk.

Acute Disease↗
PubMed1978

Type B hepatitis after transfusion with blood containing antibody to hepatitis B core antigen.

We tested the hypothesis that donor blood containing antibody to hepatitis B core antigen (anti-HBc) but lacking detectable hepatitis B surface antigen (HBsAg) and antibody (anti-HBs)might transmit Type B hepatitis by examining donor and recipient serums from a Veterans Administration study of post-transfusion hepatitis. Donor blood was available from three patients with Type B hepatitis and from one patient with hepatitis B virus infection (development of anti-HBs and anti-HBc) without symptomatic disease. All four had received 1 unit of blood with high titer of anti-HBc but lacking HBsAg and anti-HBs. In contrast, no such units had been transfused into nine patients with "immunization-like" response (development of anti-HBs without anti-HBc) or into 26 control patients. These data stress the importance of anti-HBc as an indicator of hepatitis B virus infection and support the hypothesis that high-titer anti-HBc-positive blood might be infectious.

Antibodies, Viral↗
PubMed1979

[Identification of a virus similar to hepatitis B virus in non-A non-B hepatitis].

Hepatitis B virus-like particles (including DANE particles) with DNA polymerase activity but negative for HBs Ag have been identified in NON-A, NON-B hepatitis sera positive for HC Ag. Although specifically associated with the particles, HC Ag is not a surface antigen of the hepatitis C virus identified here for the first time. The relationship of this agent with HBV seems obvious, and deserves further study.

Hepatitis B virus↗
PubMed1992

Hepatitis B virus and apparent fulminant non-A, non-B hepatitis.

While there is evidence that hepatitis C virus (HCV) does not cause fulminant non-A, non-B hepatitis, the causal agent remains unknown. To evaluate the role of hepatitis B virus (HBV) in this disease, we used a two-step polymerase chain reaction (PCR) to amplify the surface and core regions of HBV DNA in serum and liver samples taken prospectively from twenty-six patients (mean age 36 years, range 1 to 64) with acute hepatic failure undergoing liver transplantation. HBV DNA was absent from the serum of all patients before transplantation. Seventeen patients were diagnosed as having non-A, non-B hepatitis because they lacked serological evidence of hepatitis A virus or HBV infection. Liver samples were taken from twelve of these patients, and six samples were positive for HBV DNA. By contrast HBV DNA was not detected in liver from three patients with acute liver failure caused by hepatitis A or toxins. HCV RNA was not found in pretransplant samples by PCR. Four of the six patients with detectable HBV DNA in liver and presumptive non-A, non-B hepatitis had detectable HBV DNA in serum after transplantation. One additional patient who did not donate pretransplant liver had HBV DNA in a post-transplant serum sample. Thus, HBV DNA was present before or after transplantation in seven of seventeen patients with apparent non-A, non-B hepatitis. Three of five patients with detectable post-transplant serum HBV DNA were serologically positive for HBV surface antigen. These findings indicate that HBV may be a common cause of fulminant hepatic failure in patients lacking serological evidence of HBV infection.

Acute Disease↗
PubMed1992

Immunohistological study of intrahepatic expression of hepatitis B core and E antigens in chronic type B hepatitis.

AIMS: To study the intrahepatic expression of hepatitis B virus (HBV) nucleocapsid antigen; and to determine the differential distribution of hepatitis B core and E antigens in chronic hepatitis B. METHODS: Hepatocyte expression of HBV nucleocapsid antigen was studied using rabbit anti-HBc, directed against both HBcAg and HBeAg; differential distribution of HBcAg and HBeAg was studied using murine monoclonal anti-HBc and anti-HBe in 120 patients with chronic hepatitis B. RESULTS: HBV nucleocapsid antigen was detected in 14 of 16 (87.5%) HBeAg seropositive patients with chronic persistent hepatitis (CPH), and in 54 of 64 (84.4%) HBeAg seropositive patients with chronic active hepatitis (CAH). Nuclear expression of nucleocapsid antigen was more prevalent in patients with CPH than in those with CAH; this was reversed in terms of exclusive cytoplasmic expression of nucleocapsid antigen (p < 0.05). Of 45 patients with nucleocapsid antigen in the nucleus, samples from 44 (97.8%) and 17 (37.8%) stained positively with monoclonal anti-HBc and anti-HBe, respectively. Of 65 patients with cytoplasmic nucleocapsid antigen, samples from 61 (93.8%) and 57 (87.7%) stained positively with monoclonal anti-HBc and anti-HBe, respectively. CONCLUSIONS: HBV nucleocapsid antigen is more prevalent in HBeAg positive patients with CPH than in those with CAH. Cellular expression of HBcAg and HBeAg in the cytoplasm is more or less the same; in the nucleus HBcAg exceeds HBeAg expression.

Cell Nucleus↗
PubMed1977

Immune responses to the hepatitis B surface antigen and liver-specific lipoprotein in acute type B hepatitis.

A serial prospective study of cellular immunity to HBsAg and liver-specific membrane lipoprotein was undertaken in 21 adults with acute hepatitis type B. Cellular immunity to HBsAg as determined by leucocyte migration inhibition with partially purified HBsAg as antigen was detected in all the patients during the recovery phase of the illness and was already detectable at the time of admission in 13 (62%) of the cases. In five of the remaining eight the titre of HBsAg in the serum at this time was high and in the whole series there was an inverse correlation between the degree of migration inhibition on admission and the peak HBsAg titre suggesting that antigen or possibly antigen/antibody complexes might be interfering with the demonstration of cellular immunity in vitro. Using a combination of minimum migration index recorded during the recovery period peak HBsAg titre, it was possible to compute the peak aspartate aminotransferase level with reasonable accuracy, a finding consistent with the hypothesis that the severity of the illness is related to both the number of infected hepatocytes and the vigour of the immune response to HBsAg. Evidence of an immune response to the liver-specific hepatocyte membrane lipoprotein was present in 50% of the patients tested at the time of admission, but was transient, having disappeared in every case by four weeks. The minimum migration index recorded with HBsAg as antigen was significantly lower in those with detectable sensitisation to the lipoprotein and it is possible that this autoimmune reaction is also generated by the interaction of T cells with viral antigenic determinants on the liver cell surface.

Acute Disease↗
PubMed1975

Prevention of nosocomial viral hepatitis, type B (hepatitis B).

Nosocomial viral hepatitis, type B, is assuming increasing importance in the United States. The keystone to an effective hepatitis control program is surveillance of patients and personnel, especially in high-risk areas, namely dialysis units, hematology-oncology units, and laboratories. Measures to control infection are outlined for specific areas of the hospital. Data currently available suggest that employees who have persisting hepatitis B surface antigen (HBSAg) need not be removed from their positions unless they have been proved to disseminate infection. Future investigations should include methods to study: [a] the mechanisms of nonpercutaneous spread of hepatitis B virus, [b] the role of the individual with persisting HBSAg in the dissemination of hepatitis B virus, [c] the efficacy of hepatitis B immune globulin in high-risk areas, and [d] the effectiveness of various chemical and physical procedures in use for inactivation of hepatitis B virus using animal model systems.

Cross Infection↗
PubMed1992

Correlation of hepatitis B virus, hepatitis D virus and human immunodeficiency virus type I infection markers in hepatitis B surface antigen positive haemophiliacs and patients without haemophilia with clinical and histopathological outcome of hepatitis.

The hepatitis D virus (HDV) infection plays a major role in severe liver damage caused by hepatitis. To establish the prevalence of HDV infection in haemophilic patients and patients without haemophilia, 87 patients with chronic hepatitis B virus (HBV) infection were examined for serological evidence of delta hepatitis. In addition HBV, HDV and human immunodeficiency virus type 1 (HIV) infection markers were compared to clinical and histopathological outcome of hepatitis. Out of 46 haemophiliacs 30 (65%) were anti-HD-seropositive; 10 out of 30 anti-HD-positive patients (33%) had pathological liver function tests compared to 2 out of 16 anti-HD-negative haemophiliacs (13%). The rate of HIV infection did not differ between the HDV infected and the non-HDV infected individuals with haemophilia (17/27 anti-HD-positive patients versus 12/16 anti-HD-negative patients). Two haemophilic anti-HD-positive patients underwent liver biopsy, in both cases hepatitis D antigen (HDAg) was detected in the biopsies. Only 2 out of 41 patients without haemophilia were anti-HD-positive. Both had pathological liver function tests; chronic active hepatitis and cirrhosis, respectively, were diagnosed and HDAg was found in the liver biopsies. Out of 39 anti-HD-seronegative patients without haemophilia, 26 (67%) were hepatitis B e antigen positive; in the sera of 20 patients (51%) HBV-DNA was demonstrated, but only 6 patients (15%) had pathological liver function tests. In conclusion a high seroprevalence of HDV infection was found in haemophilic patients treated with non-pasteurized commercial clotting factor concentrates. An endemic spreading of HDV infection in patients without haemophilia with chronic HBV infection could not be detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1977

Hepatitis B antigen, hepatitis B antibody, and subtypes in leprosy.

The prevalence of hepatitis B antigen (HBsAg), hepatitis B antibody (HBsAb), and subtypes in 242 cases of leprosy is reported. Patients were divided into three subgroups, lepromatous (174), tuberculoid (55), and borderline (13). A total of 131 patients were tested on admission; the remaining 111 had been institutionalized for a period of 3 months or more when tested. Of the 131 cases tested on admission, 88 were retested 6 to 12 months after admission. There was no statistical difference in the incidence of HBsAg and HBsAb among the three groups or between normal controls and the leprosy patients. The predominant subtype was ADW (84.1%). After institutionalization, one lepromatous case converted to HBsAg positive and four converted to HBsAb positive.

Antibodies, Viral↗
PubMed1978

Chronic hepatitis B and hepatitis B surface antigen carriers in university students.

A study was made of latent hepatic diseases in university students. 1.4% to 1.6% of the students were positive for hepatitis B surface antigen (HBsAg), and 10.3% for anti-HBs. Of 28 students with HBs-antigenemia, 2 had chronic persistent hepatitis, and 3 minimal hepatitis, 23 being healthy carriers. Hepatitis B e-antigen (HBeAg) was detected in 44% of the students with HBsAg, and anti-HBe in 13%. Anti-HBe was significantly more frequently found in female students with HBsAg than in male students. Though most of the students with HBsAg had high titer of antibody to hepatitis B core antigen (anti-HBc), there were a small number of cases showing low titer. HBsAg and anti-HBs was detected in the same serum specimens of 2 carrier students. Liver damage was also found in 3 students without HBs-antigenemia.

Adult↗
PubMed1992

Low-dose intradermal and intramuscular vaccination against hepatitis B.

Hepatitis B and its sequelae are global problems preventable by immunization. Expense limits the use of hepatitis B vaccines, but low-dose intradermal immunization has been evaluated as a cost-saving strategy in numerous studies. With few exceptions, low-dose intradermal plasma-derived vaccines have elicited protective levels of antibody in 82%-100% of young healthy adults--a proportion similar to that noted with full-dose regimens; peak levels of antibody to hepatitis B surface antigen (HBsAg) are lower with reduced doses, however. Although children respond well to low-dose intradermal immunization, this procedure is technically difficult in neonates and should not be used for those born to HBsAg-positive mothers. For persons at high risk, antibody to HBsAg must be assessed after immunization to determine the need for a booster dose. A fourth dose 1-2 years after the initial series substantially increases antibody concentrations. In low intradermal doses, recombinant vaccine elicits lower rates of seroconversion than plasma-derived vaccine. However, low intramuscular doses of recombinant vaccine give favorable results. In short, low-dose intradermal or intramuscular immunization offers protection against hepatitis B at significant savings and may be useful for mass immunization of populations at high risk.

Hepatitis B↗
PubMed2025

Unraveling the Role of Mutations Outside the Basal Promoter and Precore Regions in the HBeAg-Negative Stage of Chronic Hepatitis B.

Hepatitis B e antigen (HBeAg) seroconversion is a crucial event in the natural history of chronic hepatitis B virus (HBV) infection, marked by a significant decrease in viral load and the emergence of mutations that suppress HBeAg expression. However, these mutations alone do not fully account for the reduction in viral load. This study investigated the biological features and pathogenic roles of mutations outside the basal core promoter (BCP) and precore regions during the HBeAg-negative stage of chronic infection. Full-length HBV genomes from HBeAg-positive (n&#x2009;=&#x2009;180) and HBeAg-negative (n&#x2009;=&#x2009;328) genotype D datasets were analyzed, revealing significantly higher genomic heterogeneity in HBeAg-negative sequences compared with HBeAg-positive genomes (50.4&#x2009;&#xb1;&#x2009;16.0 vs. 26.6&#x2009;&#xb1;&#x2009;10.5 nucleotide changes per genome). Twenty-six hotspot amino acid mutations associated with the HBeAg-negative stage were identified, with over half located in the Core region. Subsequently, full-length HBV genomes from six HBeAg-negative patient-derived serum samples were obtained by PCR amplification followed by Sanger sequencing. Infectious clones generated from these genomes, each carrying between 21 and 66 amino acid substitutions, were characterized, showing that mutations in this stage differentially affected viral fitness in vitro by up- or downregulating HBV-DNA levels (ranging from 0.2 to 5 times those of the wild-type isolate), modulating capsid assembly, and altering the expression, secretion, and subcellular localization of viral proteins. In conclusion, while mutations in the BCP and precore regions are the primary drivers of HBeAg seroconversion, mutations outside these regions significantly influence HBV biology and potentially contribute to viral pathogenicity, underscoring the complex interplay between host and virus during the HBeAg-negative stage of chronic infection.

Humans↗