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PubMedDate not supplied

Hepatitis B virus replication in acute hepatitis B, acute hepatitis B virus-hepatitis delta virus coinfection and acute hepatitis delta superinfection.

To evaluate the effect of hepatitis delta virus on the level of replication of hepatitis B virus and to assess the clinical significance that such an effect might have on the final outcome of the infection, the serological profile of hepatitis B virus DNA was investigated in 153 patients with acute or chronic hepatitis B virus infection with or without associated delta infection. Serum hepatitis B virus DNA was detected in 57% of patients with acute hepatitis B, 67% of those with acute hepatitis B virus-hepatitis delta virus coinfection and 25% of HBsAg carriers with hepatitis delta virus superinfection during the first week after the onset of symptoms. Patients with acute hepatitis B and those with acute hepatitis B virus-hepatitis delta virus coinfection did not differ significantly with respect to the serological profile of hepatitis B virus DNA and final clinical outcome. Within the group of HBsAg carriers with hepatitis delta virus superinfection, all patients who were initially negative for hepatitis B virus DNA developed chronic hepatitis delta virus infection, whereas 3 of the 4 patients with active hepatitis B virus infection at the time of superinfection showed transient inhibition of hepatitis B virus replication followed by termination of hepatitis delta virus infection in two patients. Therefore, although delta virus may inhibit the replication of hepatitis B virus among chronic HBsAg carriers, this effect is not readily apparent among patients with hepatitis B virus-hepatitis delta virus coinfection.

Acute Disease↗
PubMed1982

[Hepatitis B and hepatitis A markers in 33 cases of acute hepatitis B surface antigen-negative, hepatitis A virus antibody-positive viral hepatitis. Importance of immune complexes].

The authors have looked for the markers of HBV by R.I.A. method (HBsAg, anti HBsAg, HBeAg, anti HBeAg, anti HBcAg), of HAV (by measurement on two samples of HAVab or by measurement of HAVab IgM), the immune-complexes (I.C.C.) by C1q solid-phase binding assay method with E.L.I.S.A. with determination after division I.C.C. of HBsAg by R.I.A. method in 33 cases of HBsAg negative acute viral hepatitis. The 9% (3 cases) were HAV acute hepatitis, the 42,4% (14 cases) no A no B acute hepatitis, the 36,3% (12 case) were HBV acute hepatitis, in 9 anti HBcAg positive cases the I.C.C. with HBsAg positive after division resulted positive, the 12,3% (4 cases) had a positivity for HAVab by stereoconversion (2 cases) or HAVab IgM (2 cases) with HBsAg positivity after division I.C.C. This result puts a nosologic problem about the 4 cases of acute viral hepatitis, which, from epidemiological and clinical point of the view are HAV acute hepatitis.

Antibodies, Viral↗
PubMed1999

Etiology of sporadic acute viral hepatitis in Taiwan: the role of hepatitis C virus, hepatitis E virus and GB virus-C/hepatitis G virus in an endemic area of hepatitis A and B.

The etiology of sporadic acute hepatitis was studied in 334 consecutive patients from Taiwan (237 men and 97 women, aged 16-81 years), with emphasis on the role of hepatitis C virus (HCV), hepatitis E virus (HEV), and GB virus-C/hepatitis G virus (GBV-C/HGV) in acute non-A, non-B (NANB) hepatitis and in HBsAg carriers with superimposed acute hepatitis. According to the conventional diagnostic criteria, there were 12 cases (3.6%) of acute hepatitis A, 17 cases (5.1%) of acute hepatitis B, 128 cases (38.3%) of acute NANB hepatitis, and 177 cases (53.0%) of acute hepatitis in HBsAg carriers (those who were HBsAg positive but IgM anti-HBc negative). Among 128 cases of acute NANB hepatitis, 70 (54.7%) had acute hepatitis C (HCV RNA positive), 5 (3.9%) had acute hepatitis E (IgM anti-HEV positive), and the other 53 (41.4%) were presumably acute hepatitis non-A-E. The prevalence of acute hepatitis A, B, E, and non-A-E showed no significant sex difference, whereas acute hepatitis C was significantly more prevalent in females. The prevalence of acute hepatitis A and B decreased and that of acute hepatitis C increased significantly with increasing age. In contrast, acute hepatitis E and non-A-E showed no significant age predominance. Of 177 HBsAg carriers with acute hepatitis, 64 (36.1%) demonstrated non-B hepatotropic virus superinfection, with HCV being the most common (60.9%), followed by hepatitis D, E, and A viruses, and the other 55 (31.1%) and 58 (32.8%) were presumed to have acute exacerbation of chronic hepatitis B or superimposed acute hepatitis non-A-E, respectively. Serum GBV-C/HGV RNA was detected in 3-4% of acute hepatitis non-A-E cases, suggesting its limited role in these cases.

Acute Disease↗
PubMed1982

[Determination of hepatitis B E antigens, anti-hepatitis B E and Dane particles in the serum of hepatitis B S carriers and patients with chronic hepatitis B S antigen-positive hepatitis].

The correlation of HBeAg, anti-HBe, Dane particles and results of light microscopy of liver biopsies have been studied in 109 patients with chronic HBV infection and in 21 HBsAg carriers. The following conclusions may be drawn: 1. There is a good correlation between the presence of HBeAg and Dane particles. 2. Patients with both of these markers often have chronic active or lobular hepatitis. 3. The presence of anti-HBe points in 80% of these cases to a carriership or chronic persistent hepatitis. 4. 60% of patients without an HBe-marker and 20% of patients with anti-HBe exhibit presence of Dane particles.

Antibodies, Viral↗
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↗
PubMed1995

Simultaneous acute hepatitis B virus and hepatitis C virus infection leading to fulminant hepatitis and subsequent chronic hepatitis C.

A 22-year-old male Taiwanese was admitted to the hospital for acute hepatitis B associated with fulminant hepatic failure. After receiving supportive treatment, the patient's clinical condition improved and the results of liver function tests (including prothrombin time) gradually improved. However, in spite of seroconversion from hepatitis B surface antigen to antibody, hepatitis relapsed and serum alanine aminotransferase levels were persistently abnormal during the 3-year follow-up period. Liver biopsy performed 2 years after the onset of illness revealed chronic hepatitis. A retrospective review of the patient's serological test results revealed hepatitis C virus (HCV) RNA and the development of antibodies to HCV during the acute phase of illness as well as the persistence of HCV RNA during follow-up. Thus, we serologically and virologically proved that our patient had simultaneous acute infections with hepatitis B and C viruses and that these infections led to fulminant hepatic failure, relapse of hepatitis, and chronic hepatitis C.

Acute Disease↗
PubMed1997

Detection of hepatitis G virus RNA in patients with hepatitis B, hepatitis C, and non-A-E hepatitis by RT-PCR using multiple primer sets.

Hepatitis G virus(HGV)/GB virus C(GBV-C) is a newly identified virus associated with human hepatitis. The preliminary prevalence studies of HGV infection in Japan were entirely based on the detection of HGV RNA by RT-PCR. However, the selection of the different primer sets in such assay may influence sensitivity of the test because of the extensive genetic heterogeneity of HGV, and influence the estimation of the prevalence of HGV. To address this potential problem, we designed two primer sets from well conserved domains in the 5'NC and NS5 regions of HGV genome, and tested them together with the NS3-derived primer set in RT-PCR for their ability to detect HGV RNA in serial dilution of synthetic viral RNA templates. Subsequently, we used these three primer sets to detect HGV RNA in the sera of 371 Japanese patients with hepatitis B, hepatitis C, and non-A-E hepatitis. The results indicated that the primer set derived from the 5'NC region appeared to be most effective in detecting HGV RNA. The results also showed that only two out of the 126 patients (1.6%) with non-A-E hepatitis were positive for HGV RNA although the RNA were detected more frequently in patients with hepatitis B (2/38; 5.3%) and hepatitis C (17/207; 8.2%), suggesting that HGV is not a common causative agent for non-A-E hepatitis in Japan.

Base Sequence↗
PubMed1999

Genetic alterations in the S gene of hepatitis B virus in patients with acute hepatitis B, chronic hepatitis B and hepatitis B liver cirrhosis before and after liver transplantation.

BACKGROUND: Several studies have shown that hepatitis B immunoglobulin (HBIG) imposes a selection pressure on the hepatitis B virus (HBV) S gene, and that the emergence of mutations in this region would make reinfection after orthotopic liver transplantation (OLT) possible. AIMS: This study was undertaken to analyze the presence of HBV S-gene mutations in the different stages of HBV infection and the relationship between HBIG therapy and the emergence of mutations in liver transplant recipients. METHODS: The frequency and location of mutations in the coding region of the HBV S gene were studied by PCR and direct sequencing in 30 patients (7 with acute self-limited hepatitis B, 16 with chronic hepatitis B and 7 recipients of (OLT) for HBV-related end stage liver disease who became reinfected). RESULTS: The average number of amino acid changes was higher in patients with a more advanced stage of disease, 0.57 mutations/100 positions in acute hepatitis B and 1.57 in chronic hepatitis B (1.28 in HBeAg-positive and 1.8 in anti-HBe-positive patients). The average number of substitutions in the transplanted patients was 2.7 before OLT and 3 after OLT. No amino acid substitutions were detected in the "a" determinant of HBsAg in acute hepatitis B, however, 8 substitutions were observed in 6 chronic patients. In 3 OLT patients, 4 substitutions were observed in samples before and after OLT. One of these patients, who had protective levels of anti-HBs, showed 3 additional new amino acid substitutions after OLT, suggesting escape mutant selection by the effect of HBIG therapy. No changes were observed between the consensus sequences obtained several years before and after transplantation, indicating consensus sequence stability. CONCLUSION: These results show that there is an accumulation of HBV S-gene mutations in HBV-related end-stage liver disease. Prophylaxis with HBIG mainly obtained from acute self-limited hepatitis patients who have a highly homogeneous viral population, may be one factor underlying the reinfection after liver transplantation.

Acute Disease↗
PubMed1987

Correlation between hepatic hepatitis B core antigen and serum hepatitis B virus-DNA levels in patients with chronic hepatitis B virus infections in Taiwan.

Paired liver biopsy specimens and serum samples from 76 patients with chronic hepatitis B virus (HBV) infection were taken for staining of hepatitis B core antigen (HBcAg) by immunoperoxidase and testing of HBV-DNA by a spot hybridization technique, respectively. Thirty-two tissue specimens showed positive staining for HBcAg in their hepatocytes. The two patients with diffuse HBcAg expression in liver tissue also had high serum concentrations of HBV-DNA (greater than 10 pg/10 microL). Among 30 patients with focal HBcAg distribution, 28 patients (93.3%) had measurable levels of serum HBV-DNA and 17 patients (60.7%) had high levels of serum HBV-DNA. Of 44 patients without hepatic HBcAg expression, only 12 patients (27.3%) had detectable serum HBV-DNA, and most patients (93.1% [11/12]) had low concentrations (less than 10 pg/10 microL). Nineteen patients had superimposed hepatitis D virus infection, and, of these, three patients (15.8%) had detectable serum HBV-DNA in low concentrations, while one of the three patients had stainable HBcAg in his hepatocytes with focal distribution. Two of the three patients with hepatitis A virus superinfection who had focal HBcAg expression in their liver tissue had serum HBV-DNA levels that were high during the acute phase of hepatitis A virus infection, and in one patient his serum HBV-DNA levels further increased from 10 pg/10 microL to 40 pg/10 microL during the recovery phase. Thus, measurement of serum HBV-DNA levels in patients with chronic HBV infection correlated well with their hepatic HBcAg expression, and both represent the precise status of HBV replication.

Adolescent↗
PubMed1986

Chronic hepatitis B. Impact of hepatitis D virus superinfection and the hepatitis B e-system on histological outcome, and correlation of the hepatitis B e-system to HBV-DNA in serum.

Chronic evolution after acute hepatitis B virus infection. During a 13 months period 1977-1978 a total of 129 cases of acute viral hepatitis type B occurred among patients who were admitted with hepatitis to Roslagstull, Hospital, Stockholm, Sweden. Less than 1% progressed to chronicity. Prevalence of Delta superinfection was studied among 60 patients with chronic hepatitis B. Nineteen (32%) were anti-delta positive. The majority of the positive patients were either non-European immigrants or addicts, both 9/19 (47%). Infections with the delta agent was found to have occurred in Stockholm already in the early 1970s. Rate of HBeAg clearance during chronic HBV was studied among 36 HBeAg positive patients. Seroconversion to anti-HBe was noted in 17 patients (47%), whereas HBeAg persisted in 19 during a mean follow-up period of 53 months. The spontaneous annual HBeAg seroconversion rate was 11%. HBeAg clearance occurred as frequently among homosexual men as among patients in other categories. However, 12/14 homosexual men were HBeAg positive after 2 years follow-up, compared with 1/13 drug addicts. Thus, homosexual men seemed to require a longer time for HBeAg seroconversion than i.v. drug addicts. HBV-DNA in serum, a strong indicator of viral particles and infectivity was analysed among patients with HBeAg seroconversion, initial HBeAg negativity and/or delta superinfection. HBV-DNA was found in 75-80% of our HBeAg positive patients. A correlation between chronic liver disease and presence of HBV-DNA in serum was also found. Thus, HBV DNA was found in 63% of patients with CAH or CAH/CI as compared with only 39% of patients with CPH. Delta infected patients had HBV-DNA more often than those without hepatitis D infection. Seven delta infected, anti-HBe positive, patients were still HBV-DNA positive five to eight years later. Therefore delta infected anti-HBe positive patients can be infectious for prolonged periods. Histological outcome. 63% (12/19) anti-delta positive patients were classified as CAH with or without cirrhosis as against 39% (16/41) of the anti-delta negative patients. Eleven of 15 homosexual men (73%) had histological findings classified as CAH or CAH/CI. None of them were superinfected with HDV. Thus homosexual men developed severe hepatic lesions without being delta infected. In contrast 78% (7/9) i.v. drug addicts with CAH were delta infected. A numerical scoring system was applied and compared with conventional morphological classification of liver histology to assess the histological outcome of 42 patients with repetitive liver biopsies.

Acute Disease↗
PubMed1993

Absence of hepatitis B virus DNA detected by polymerase chain reaction in blood donors who are hepatitis B surface antigen negative and antibody to hepatitis B core antigen positive from a United States population with a low prevalence of hepatitis B serologic markers.

A recent study in hepatitis B surface antigen (HBsAg)-negative, antibody to hepatitis B core antigen (anti-HBc)-positive blood donors from a population with a high prevalence of hepatitis B serologic markers showed the presence of hepatitis B virus DNA (HBV DNA) as detected by polymerase chain reaction (PCR) in 4 percent of these donors. A sensitive, nested PCR assay was used to assess the prevalence of HBV DNA in a population of HBsAg-negative, anti-HBc-positive blood donors from a United States population with a low prevalence of hepatitis B serologic markers. The lower limit for detection by the PCR assay was 10(-5) pg per mL of HBV DNA. There was a review of 26,492 consecutive blood donations in a 12-month period. During this time, only 1 unit (0.004%) was HBsAg positive. An additional 158 units (0.6%) were repeatably reactive for anti-HBc. These 158 HBsAg-negative, anti-HBc-positive units were given by 119 donors of blood for allogeneic and autologous use. HBV DNA was not detected by PCR in blood from 83 allogeneic blood donors (93 samples) or 36 autologous blood donors (65 samples). Anti-HBc testing is an inefficient means of screening for potential hepatitis B infectivity and is associated with low test specificity in populations with a low prevalence of hepatitis B serologic markers.

Adolescent↗
PubMed1998

Interferon treatment in hepatitis B surface antigen-positive hepatitis B e antibody-positive chronic hepatitis B: role of hepatitis B core antibody IgM titre in patient selection and treatment monitoring.

Chronic hepatitis B infection with the hepatitis B e antigen (HBeAg)-negative variant is associated with a severe clinical course and a low response rate to interferon (IFN). In an attempt to improve the chances of sustained response to interferon we designed a pilot study, using titres of IgM antibodies to hepatitis B core antigen (HBcAb IgM) to guide treatment initiation. Eighteen adults who were HBeAg-negative with biopsy-proven chronic active hepatitis (seven with cirrhosis) entered the study. They were followed-up bimonthly with routine liver function tests, and HBcAb IgM titres were also determined. Treatment (lymphoblastoid IFN 5 million units (MU) m(-2) three times weekly for 6 months) was started when the HBcAb IgM titre was increasing. Fifteen (83.3%) patients had normal alanine aminotransferase (ALT) levels and undetectable HBV DNA at the end of treatment. HBcAb IgM decreased in all responders. We observed a relapse in four patients (three with cirrhosis), in the first year after treatment, with an increase in ALT, HBV DNA and titre of HBcAb IgM. Eleven patients (61.1%) had a sustained response and eight of these 11 patients were followed-up for more than 18 months; two responders cleared hepatitis B surface antigen (HBsAg). Hence, the rate of sustained response to IFN in HBeAb-positive patients with chronic hepatitis is improved if treatment is started when HBcAb IgM levels are increasing.

Adolescent↗
PubMed2000

Autoimmune forms of chronic hepatitis associated with hepatitis C virus (HCV) infection with and without HCV-RNA: histological differences from pure autoimmune hepatitis and chronic hepatitis C.

Liver biopsy specimens of pure autoimmune hepatitis (pAIH), autoimmune forms of chronic hepatitis with positivity for anti-hepatitis C virus (anti-HCV) and negativity for HCV-RNA (cAIH-RNA(-)), autoimmune forms of chronic hepatitis with positivity for anti-HCV and HCV-RNA (cAIH-RNA(+)), and chronic hepatitis C (CHC) were compared histologically and statistically to clarify the histological character of the autoimmune form of chronic hepatitis with HCV infection. The following representative histological features were used to investigate: inflammation, fibrosis, plasma cell infiltration, lymphoid aggregates/follicles, non-suppurative destructive cholangitis, and the shape of the enlarged portal tracts. While a considerable overlap in histological features between the pAIH and cAIH-RNA(-) groups and between the CHC and cAIH-RNA(+) groups was recognized, the overlap between the pAIH and CHC groups was small. Significant differences were found between cAIH-RNA(-) and cAIH-RAN(+) groups, especially in necroinflammatory findings. In conclusion, most cases of cAIH-RNA(-) with histological features similar to those of pAIH were shown to be AIH. The remaining cases might be CHC with subsidence of viral duplication. Conversely, many cases of cAIH-RNA(+) with histological findings similar to those of CHC were shown to be CHC clinically mimicking pAIH. The remaining cases might represent coexistence of pAIH and HCV infection.

Antibodies, Antinuclear↗
PubMed2000

Acute hepatitis A and acquired immunity to hepatitis A virus in hepatitis B virus (HBV) carriers and in HBV- or hepatitis C virus-related chronic liver diseases in Thailand.

A number of studies have suggested that the clinical course of hepatitis A virus (HAV) infection is more severe in patients with chronic liver disease (CLD). A study was undertaken to determine the impact of acute HAV in asymptomatic hepatitis B surface antigen (HBsAg) carriers (n = 20) and patients with hepatitis B virus (HBV)-(n = 8) or hepatitis C virus (HCV)-related (n = 4) CLD. Disease progression was compared with that in 100 patients with isolated HAV infection. No patient with HAV infection alone developed complications, and all recovered fully. Fulminant or submassive hepatitis occurred in 55% of HBsAg carriers and 33% of patients with HBV- or HCV-related CLD. The mortality rate in HBsAg carriers (25%) was not significantly different from that in the patients with CLD (33%). The seroprevalence of anti-HAV immunoglobulin G in 820 individuals was also determined. Approximately 50% of the individuals had acquired HAV infection between the ages of 21 and 30 years. It was demonstrated that HAV infection may have a more severe clinical course in patients with underlying CLD, particularly among older individuals. Vaccination for such patients should be considered.

Acute Disease↗
PubMed1995

Failure to incriminate hepatitis B, hepatitis C, and hepatitis E viruses in the aetiology of fulminant non-A non-B hepatitis.

Sporadic non-A, non-B hepatitis is the most common indication for liver transplantation in patients presenting with fulminant and subacute liver failure. This study used serological, histological, and molecular biological techniques to examine specimens from 23 consecutive patients transplanted for sporadic non-A, non-B hepatitis. No evidence was found of hepatitis C virus, hepatitis E virus, or 'cryptic' hepatitis B virus infection.

Adolescent↗
PubMed1991

Effect of screening for hepatitis C virus antibody and hepatitis B virus core antibody on incidence of post-transfusion hepatitis. Japanese Red Cross Non-A, Non-B Hepatitis Research Group.

Since November 1989, Japanese Red Cross blood centres throughout the country have screened donors for hepatitis C virus (HCV) with an Ortho enzyme-linked immunosorbent assay for antibody to the C100-3 viral peptide. Simultaneously, the centres started to screen for units with high-titre (greater than or equal to 2(6)) antibody to hepatitis B virus core antigen (HBcAb) in the absence of hepatitis B virus surface antigen and antibody. To test the effectiveness of this policy, the incidence of post-transfusion non-A, non-B hepatitis (PTNANBH) and post-transfusion hepatitis B (PTHB) after screening had been introduced (November, 1989, to December, 1990, inclusive) was compared with the incidence before screening (January, 1988, to October, 1989, inclusive). Incidence of PTNANBH in patients who had received 1-10 unit transfusions was 4.9% (58/1189) before screening vs 1.9% (15/784) afterwards. Incidence in those who had 11-20 unit transfusions was 16.3% (64/392) vs 3.3% (4/124). Incidence of PTHB was 0.25% (4/1597) before screening; no cases have been detected subsequently. These results show the effectiveness of the first-generation anti-HCV test and indicate the value of screening for high-titre HBcAb in addition to HBV surface antigen testing in HBV endemic areas.

Alanine Transaminase↗
PubMed1988

Hepatitis B virus infection and hepatocellular carcinoma: correlation between IgM antibody to hepatitis B core antigen, hepatitis B e antigen, and hepatitis B DNA.

Sera from 102 black patients with primary hepatocellular carcinoma (PHC) and hepatitis B surface antigenemia were tested for immunoglobulin M antibody against hepatitis B core (IgM anti-HBc), hepatitis B e antigen (HBeAg), and hepatitis B viral (HBV) DNA. Their prevalences were compared to those of a control group of 124 age and sex matched black HBV carriers without tumor. IgM anti-HBc was present in 68.6%, HBeAg in 32.3%, and HBV-DNA in 26.7% of the patients. In the control population, IgM anti-HBc was present in 45%, HBeAg was detected in 3.2%, and HBV-DNA in 25.8%. We conclude that IgM anti-HBc is present appreciably more often than either HBeAg or HBV-DNA in patients with PHC. HBeAg or IgM anti-HBc in serum of HBsAg positive carriers may predict an added risk of PHC development in South African blacks.

Adolescent↗
PubMed1995

Proliferative response of CD4+ T cells and hepatitis B virus clearance in chronic hepatitis with or without hepatitis B e-minus hepatitis B virus mutants.

To assess the significance of cell-mediated immunity, T cells were derived from the peripheral blood and liver tissue of hepatitis B virus (HBV)-infected patients and controls. The analysis of the 3H-thymidine-uptake in response to a panel of recombinant HBV antigens revealed that peripheral blood mononuclear cells (PBMC) of the 25 viremic patients with inflammatory active, chronic hepatitis B, 16 with wild-type and nine with HBe-minus HBV mutant infection, showed stronger proliferative responses to HBc and HBe antigens than 16 asymptomatic nonviremic HBsAg carriers with normal aminotransferase levels (HBc: SI 19.3 +/- 3.9 vs. 13.0 +/- 3.2 vs. 8.0 +/- 1.2; P < .01 and HBe: SI 16.6 +/- 4.0 vs. 10.7 +/- 3.5 vs. 6.9 +/- 1.5; P < .05). In 15 patients with acute self-limited hepatitis B, however, significantly stronger HBc antigen-specific T-cell responses were observed during HBV clearance and HBe/anti-HBe seroconversion, whereas in nine completely HBV-immunized patients only minor proliferative responses to HBV antigens were observed. Six HBe/HBcAg- and two HBeAg-specific CD4+ T-cell lines could be expanded from liver tissue and peripheral blood of six viremic patients with chronic hepatitis B. Irrespectively of HBV mutations the HBV-specific activation of the T-cell lines was restricted by the presence of HLA-DR molecules and resulted in the release of Th1-like cytokine patterns. Follow-up of interferon (IFN) recipients showed simultaneous short-term increase of HBc/HBe-specific T-cell reactivities in responder patients during HBV clearance and HBe/anti-HBe seroconversion, whereas in nonresponders high virus load and HBV-specific immune responses were in imbalance.(ABSTRACT TRUNCATED AT 250 WORDS)

CD4-Positive T-Lymphocytes↗