Biomedical subjects

H Norder

Publications and source records attributed to H Norder.

At least 37 records · Page 2Linked to original sources

PubMed1995

Nosocomial spread of hepatitis B virus (HBV) in a haemodialysis unit confirmed by HBV DNA sequencing.

An outbreak of hepatitis B virus (HBV) infection in a haemodialysis unit is described. Four patients in the unit contracted subclinical HBV infection within three months. DNA sequence analysis of the S gene of HBV isolates from chronic carriers and newly infected patients in the unit aided in tracing possible transmission pathways. Three newly infected patients had received partial or complete HBV vaccination previously. HBV was rapidly cleared from all three although the anti-HBs titre had not reached 10 IU L-1 in any of them at the time of infection.

Cross Infection↗

PubMed1995

Subtypes, genotypes and molecular epidemiology of the hepatitis B virus as reflected by sequence variability of the S-gene.

The serologic heterogeneity of the hepatitis B virus (HBV) has been established from immunodiffusion experiments for a long time. Four serotypes called subtypes of the hepatitis B surface antigen (HBsAg) have been defined by two mutually exclusive determinant pairs, d/y and w/r, and a common determinant a. These subtypes are adw, ayw, adr and ayr. By subdivision of the four major subtypes in the mid-70s, nine different subtypes were identified. Sequencing of viral genomes has now become a major goal of descriptive virology, and sequence data is now used to trace routes of infection, to reconstruct the phylogenetic history of viruses and two delimit genetic subtypes. A genetic classification based on the comparison of complete genomes has defined four genomic groups of HBV, later referred upon as genotypes, which were designated with A-D. However, the interrelation of the nine subtypes to the genotypes, the possible presence of more than four human HBV genotypes as well as their global geographical prevalence remained to be determined. By sequencing the S-gene of HBV the molecular basis was assessed for the serological variations of HBsAg within the major four subtypes. Thereby, also two new genotypes of HBV designated with E and F were identified. Complete genomic sequencing of E and F strains confirmed their status as new genotypes. The F genotype was found to diverge from other HBV genomes sequenced by 14%, thus being the most divergent HBV genome so far characterized. When the worldwide molecular epidemiology of HBV based on the variability of the S-gene was defined, the E and F strains seemed to originate in aboriginal populations of Africa and the New World, respectively. They shared a unique substitution at residue 140 in the second immunodominant loop of their encoded surface antigen when compared to the vaccine strain. Future research will establish whether this substitution may predispose to a vaccine escape mutant at residue 141, that now has been reported to occur in conjunction with the 140 substitution.

Demography↗

PubMed1994

Complete genomes, phylogenetic relatedness, and structural proteins of six strains of the hepatitis B virus, four of which represent two new genotypes.

The genomes of six hepatitis B viral (HBV) strains were sequenced from 10 overlapping amplificates obtained by the polymerase chain reaction. Four of the strains, specifying subtypes ayw4 and adw4q-, represented on the basis of divergency within the S gene two new genomic groups identified by us. The other two strains, encoding adrq- and of Pacific origin, belonged to genomic group C. The relation of these genomes to 21 published human, 1 chimpanzee, and 4 rodent hepadnaviral genomes was analyzed by constructing a phylogenetic dendrogram. Thereby, the segregation of human HBV strains into six genomic groups was confirmed. A consistent grouping of the genomes compared was also obtained in dendrograms based on the P and S genes, although the branching order differed from that based on the entire genomes. Each of the two representatives of genomic groups E and F differed by 8.1 to 13.6% and by 12.8 to 15.5% from the genomes of the other groups and by 1.5 and 3.7% from each other. The two Pacific group C strains differed by 2.7% from each other and by 4.1 to 5.4% from other group C genomes, suggesting that they diverged early from the other group C genomes. The F strains formed the most divergent group of HBV genomes, which may be explained by their representing the original strains of the New World. Within the structural gene products, 17 and 34 amino acids unique for human HBV strains were recorded in the sequenced E and F strains, respectively. Most notable is the Ser81 to Ala81 substitution in an immunodominant region of HBcAg, and the four extra cysteine residues in HBsAg at residues 19, 183, 206, and 220, which might be engaged in additional disulphide bridges. Five residues shared by E and F strains were also unique for human HBV strains. Two of these, Leu127 and Ser140 in HBsAg, were the only substitutions that may explain the w4 reactivity shared by these HBV strains. Interestingly, the Ser140 substitution occurs in an immunodominant loop of the a determinant claimed to be important for the protective immune response to HBV vaccination.

Amino Acid Sequence↗

PubMed1994

Contrasting roles of rivers and wells as sources of drinking water on attack and fatality rates in a hepatitis E epidemic in Somalia.

In early 1988, an increased incidence of acute hepatitis was observed in villages along the Shebeli River in the Lower Shebeli region of Somalia. This was followed by a large epidemic that lasted until late 1989. In a survey of 142 villages with a population of 245,312 individuals, 11,413 icteric cases were recorded, of which 346 died, corresponding to an attack rate and a case fatality rate of 4.6% and 3.0%, respectively. The etiologic role of hepatitis E virus (HEV) in this epidemic was proven by demonstrating anti-HEV in 128 of 145 sampled cases as a sign of recent infection with HEV. In three villages, where a special study protocol was implemented, the attack rate was found to increase significantly with age from 5% in the group 1-4 years of age to 13% in the group 5-15 years of age and to 20% for persons older than 15 years of age. Among cases 20-39 years of age, the female-to-male ratio was 1.5:1, which was a significant predominance of females. As in other hepatitis E outbreaks, there was a high fatality rate in pregnant females, estimated to be 13.8%. The epidemic peaked with the rise in the level of the river during rainfall, suggesting that the disease was waterborne. The attack rate was higher (6.0%) in villages supplied with river water, while fewer cases were recorded in those relying on wells or ponds for their water supply, 1.7% and 1.2%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1993

Complete nucleotide sequences of six hepatitis B viral genomes encoding the surface antigen subtypes ayw4, adw4q-, and adrq- and their phylogenetic classification.

The complete nucleotide sequences of six hepatitis B viral (HBV) genomes were determined by dideoxy chain termination sequencing of ten overlapping nucleotide fragments obtained by the polymerase chain reaction. Four of the genomes belonged to the two genomic groups E and F of HBV which have been previously identified by us on the basis of sequence divergences within the S gene. Genomic group E encodes the HBsAg subtype ayw4, group F adw4q-. The other two genomes were of Pacific origin within group C and encoded adrq-. The relationship of these complete human HBV genomes to 21 that have been previously published, together with one chimpanzee virus and four rodent hepadnaviral genomes, was investigated by constructing a phylogenetic tree utilizing a combination of distance matrix and approximate parsimonious methods. Thereby, the previously demonstrated segregation of human HBV strains into six genomic groups was confirmed. Both of the representatives of the groups E and F were found to differ by 8.1-13.6% and by 12.8-15.5% from the genomes of the other genomic groups and by 1.5 and 3.7% from each other. Since they differed by more than 8% from the genomes in the other groups, the limit originally used to define HBV, genomic groups their status as new genomic groups was confirmed. The two Pacific group C strains were found to differ by 2.7% from each other and by 4.1 to 5.4% from other group C genomes, suggesting that they diverged early from the other group C genomes. According to both the overall similarity and the phylogenetic dendrogram the F strains formed the most divergent cluster of HBV genomes favoring the concept that they represented the original HBV strains of the New World. The next split in the dendrogram segregated the A, D, E and the chimpanzee strains from the Asian B and C strains. Information on the nucleotide sequences and their encoded products of HBV strains of different genomic groups will provide a basis to understand biological variations of the HBV infection in different parts of the world.

Animals↗

PubMed1993

Severe aplastic anemia associated with seronegative community-acquired hepatitis C virus infection.

Aplastic anemia (AA) is a rare complication of viral hepatitis affecting mainly children or young adults. Most reported cases have been associated with community-acquired non-A, non-B hepatitis, but hepatitis A and B have also been implicated in a few patients. We report on a 43-year-old woman with severe AA, in association with acute hepatitis C virus (HCV) infection, diagnosed by detection of HCV RNA by the polymerase chain reaction technique. Her AA was successfully treated with anti-thymocyte globulin and cyclosporin A. The hepatitis C progressed to chronic disease but, despite a follow-up time of 2 years, the patient still has no detectable anti-HCV antibodies, as evaluated with a second-generation anti-HCV assay.

Adult↗

PubMed1993

Late seroconversion and high chronicity rate of hepatitis C virus infection in patients with hematologic disorders.

BACKGROUND: Patients with hematologic disorders requiring repeated blood and platelet transfusions are at high risk for development of post-transfusion non-A, non-B hepatitis. PATIENTS AND METHODS: Fifty-five patients with hematologic diseases and post-transfusion non-A, non-B hepatitis were studied. Sera were assayed for hepatitis C virus (HCV) antibodies with a second-generation enzyme-linked immunoassay. Sera from 40 patients were examined for the presence of HCV RNA with a nested PCR method. RESULTS: The clinical picture of acute non-A, non-B hepatitis did not differ from that described in other patient groups: however, progression to chronic hepatitis was very common (95%). Thirty-eight (95%) of 40 patients, whose sera were analysed both serologically and for the presence of HCV RNA had verified HCV infections. In some patients time to seroconversion was prolonged, up to more than 14 months. Seventeen patients with resistant or relapsed acute leukemia were treated with combination chemotherapy during the acute or chronic phase of hepatitis. Suppression of the inflammatory activity as reflected by a decrease of serum aminotransferase levels was recorded during the subsequent pancytopenic period. CONCLUSIONS: Hepatitis C has a high chronicity rate in patients with hematologic disorders which parallels the situation of hepatitis B in the immunocompromised host. Furthermore, like the situation in hepatitis B, the hosts' immune response to infection seems to be involved in the pathogenesis of liver injury. Time to seroconversion may be prolonged and detection of HCV RNA is therefore important for diagnosis.

Adolescent↗

PubMed1993

Genetic relatedness of hepatitis B viral strains of diverse geographical origin and natural variations in the primary structure of the surface antigen.

A 681 nucleotide fragment of the hepatitis B virus (HBV) genome was sequenced that corresponded to the complete gene for hepatitis B surface antigen (HBsAg) in 80 HBsAg- and hepatitis B e antigen (HBeAg)-positive sera of diverse geographical origins. These and 42 previously published HBV sequences within the S gene were used for the construction of a dendrogram. In this comparison, each of the 122 HBsAg genes was found to be related to one or other of the six previously identified genomic groups of HBV, A to F. The HBV strains within each genomic group showed a characteristic geographical distribution. Group A genomes were represented by 23 strains mainly originating in northern Europe and sub-Saharan Africa. The group B and C genomes, represented by 17 and 28 strains respectively, were confined to populations with origins in eastern Asia and the Far East. The group D genomes, represented by 38 strains, were found worldwide, but were the predominant strains in the Mediterranean area, the Near and Middle East, and in south Asia. Group E genomes, represented by nine strains, were indigenous to western sub-Saharan Africa as far south as Angola. There were indications that the F group, made up of six strains, represented the genomic group of HBV among populations with origins in the New World. Thus, HBV has diverged into genomic groups according to the distribution of mankind in the different continents. As well as giving information on the genetic relationship of HBV strains of different geographical origin, this study also provides information on the primary structure of HBsAg in different regions of the world. Such data might prove valuable in explaining the reported failures to obtain protection with current HBV vaccines.

Amino Acid Sequence↗

PubMed1993

Important role of hepatitis C virus infection as a cause of chronic liver disease in Somalia.

In a case-control study, 62 Somali patients with chronic liver disease (CLD) including primary hepatocellular carcinoma (HCC) and the same number of age and sex matched controls were investigated for serological markers of hepatitis C virus (HCV) and hepatitis B virus (HBV) infections. Antibody to HCV (anti-HCV) was detected in 40.3% and 6.5% of cases and controls, respectively. The corresponding prevalences of hepatitis B surface antigen (HBsAg) were 37.1% and 9.7%, respectively. Of the HBsAg-positive cases, 34.6% had antibodies to hepatitis D virus (anti-HD) compared with 14.3% among the HBsAg-positive controls. Anti-HCV was less prevalent in HBsAg-positive cases than among HBsAg-negative patients (p < 0.001), indicating that these agents were independent causes of CLD/HCC. The odds ratios for patients with CLD/HCC associated with the presence of anti-HCV, anti-HD, HBsAg without anti-HD and anti-HCV, were found to be 9.8, 10.4, and 3.3, respectively. When the patients were divided into tumour and non-tumour cases, using the criteria of serum alpha-fetoprotein > 100 ng/ml and/or solid hepatic lesions detected by ultrasonography, they did not differ with regard to frequencies of HBsAg and/or anti-HCV, although they did differ when these markers were taken together (43/49 versus 5/13, respectively). The mean age of the tumour patients with anti-HCV alone was significantly higher than that of tumour patients with HBsAg as the sole marker, 61.7 versus 31.4 years (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Interferon alpha-2b treatment in an HIV-infected patient with hepatitis B virus induced nephrotic syndrome.

A 31-year-old male patient with an asymptomatic HIV infection but with a hepatitis B (HBV) related membraneous glomerulonephritis with nephrotic syndrome was given interferon alpha-2b subcutaneously 3 times weekly for 7.5 months. Zidovudine was added at the 10th week due to low CD4+ cell counts. Before the 6th week of treatment the patient reported a reduced need for diuretics to keep his lower limb edemas at a minimum. This response was partially sustained even after the 7.5 months interferon treatment course. The titers of HBV-DNA decreased markedly during the treatment with interferon but rose to pretreatment levels after discontinuation of the interferon treatment. The serum albumin increased but the proteinuria and hematuria were unaffected. Adverse reactions like fever, myalgias and anemia were tolerable and did not require dose reduction of either interferon or zidovudine. This treatment regimen, at least temporarily, improved the situation for the patient and can be worthwhile to try in HIV-infected patients with HBV related nephritis with nephrotic syndrome.

Adult↗

PubMed1992

Detection of HBV DNA by PCR in serum from an HBsAg negative blood donor implicated in cases of post-transfusion hepatitis B.

An HBsAg negative blood donor, and three of her recipients, who developed HBsAg positive post-transfusion hepatitis B, were all positive for serum HBV DNA by polymerase chain reaction (PCR), and by subtype discriminating PCR were found to harbour HBV specifying ayw. Thus HBV specifying ayw. Thus HBV DNA may be detected and sub-typed by PCR in infectious HBsAg negative individuals.

Base Sequence↗

PubMed1992

HBcAg induced T-cell independent anti-HBc production in chronic HBsAg carriers.

The capacity of the nucleocapsid protein of HBV to function as a T-cell independent antigen in man was studied. When T-cell depleted B-cell cultures were challenged with E coli-derived HBcAg, anti-HBc production was registered in culture supernatants from the majority of chronic HBsAg carriers in a quiescent stage of disease. In contrast, similarly prepared and stimulated cultures from donors with natural acquired immunity to hepatitis B or HB-susceptible controls were non-responsive. Addition of autologous T-cells effectively restored anti-HBc responsiveness in T-cell depleted B-cell cultures from HB-immune donors, demonstrating the T-cell dependency for anti-HBc induction in natural HBV-infection.

B-Lymphocytes↗

PubMed1992

Molecular basis of hepatitis B virus serotype variations within the four major subtypes.

Amino acid residues 101 to 180 of hepatitis B surface antigen (HBsAg) were predicted by sequencing the corresponding part of the S gene of hepatitis B virus (HBV) DNA in 46 HBsAg-positive sera, which had been subtyped by immunodiffusion with respect to d/y, w/r, w1 to w4 and q. The sequences of the nine different HBV serotypes defined by these specificities were found to be homogeneous proving that they represent consistent variations of HBV at the genomic level. Residue 127 was found to be important as were Pro, Thr and Leu for w1/w2, w3 and w4, respectively. Five residues were found to differ between ayw1 and ayw2. These were at positions 134 (Phe instead of Tyr), 143 (Thr instead of Ser), 159 (Ala instead of Gly), 161 (Tyr instead of Phe) and 168 (Val instead of Ala). However, all these residues were shared by ayw1 and adw2, implying that Arg122 was also important for w1 expression. All genomes expressing r, apart from one ayr strain, had an Ile126, which might explain the pseudo-allelism of w1 to w4 in relation to r, since this substitution might influence the w epitope. There were two regions where adw4q- and adrq- differed from all the q+ subtypes. These were located at residues 158 and 159, and at residues 177 and 178, where both the q- subtypes had amino acid substitutions in adjacent positions. The mapping of the epitopes defining these antigenic specificities will help to link information on the world-wide distribution of HBsAg subtypes to future molecular epidemiology with regard to HBV.

Amino Acid Sequence↗

PubMed1992

Comparison of the amino acid sequences of nine different serotypes of hepatitis B surface antigen and genomic classification of the corresponding hepatitis B virus strains.

The surface (S) genes of 12 hepatitis B viruses (HBVs) encoding nine different serotypes of hepatitis B surface antigen (HBsAg) were amplified by the polymerase chain reaction and sequenced. These represented the eight strains of HBV, P1 to P8, defined at an international workshop on HBsAg subtypes in Paris in 1975, and the adrq- subtype. The S genes from additional HBV strains, one ayw4, one adw4 and one ayw1, of sub-Saharan African origin, were also sequenced. The relationship of these 12 new S gene sequences to those of the 20 published previously was investigated by constructing a phylogenetic tree, which confirmed a previous classification into four groups, designated A to D, based on 18 complete HBV genomes. When relating our sequenced S genes to these genomic groups, ayw1 of African origin and P6 (adw2) were both allocated to group A, the reference P1 (ayw1 of Vietnamese origin) was allocated to group B, P5 (ayr), P8 (adr) and adrq- were all related to group C, and P2 (ayw2) and P3 (ayw3) could both be allocated to group D. Interestingly, the S genes of w4 serotype viruses, i.e. P4 (ayw4) and P7 (adw4q-), differed by 4% or more from both previous groups and from each other, suggesting their classification into two new groups, for which the designations E and F are proposed. Genomes specifying ayw were also found in groups A and B; previously sequenced genomes specifying the ayw subtype have all been confined to group D. There were indications that the epitope for subdeterminants of w resided at amino acid positions 125 to 127. Thus, at positions 125 and 127, ayw1, ayw2 and adw2 had T and P residues, respectively, whereas M and T residues were at the corresponding positions of ayw3. Both ayw4 and adw4 had L at residue 127, and all strains expressing r, apart from P5, had an I instead of a T residue at position 126.

Amino Acid Sequence↗

PubMed1992

The risk for hepatitis A, B, and C at two institutions for children in Somalia with different socioeconomic conditions.

The prevalence of serologic markers for hepatitis A, B, and C was investigated in children from two residential institutions in Somalia. Among 596 individuals at one residence (Shebeli), the prevalences were 96% for antibody to hepatitis A virus (anti-HAV), 75% for total hepatitis B virus (HBV) markers, 16% for hepatitis B surface antigen (HBsAg), and 1.5% for antibody to hepatitis C virus (anti-HCV). Corresponding figures for the 76 individuals at a smaller residence (Societe Organisation Sociale, SOS) were 59%, 20%, 3.9%, and 0%, respectively. At Shebeli, the HBsAg carrier rates in the 1-10-year-old age group was 28% for boys and 16% for girls. These rates were significantly higher than in the older children (16% and 7.4% for boys and girls, respectively). Fifty-eight percent of the HBsAg carriers were positive for hepatitis B e antigen. Total HBV markers were significantly more frequent in girls from Shebeli, when their duration of residence was longer than five years (89% versus 63%). The duration of stay did not influence the prevalences of HBsAg, HAV, or HCV antibodies. A followup study of children initially seronegative for HBV markers was carried out after two years. For children at Shebeli 1-10 years old, the annual seroconversion rates to HBV markers (95% confidence interval) was 60.5% (42.7-77.0%). The corresponding rate for children at SOS was 10.2% (5.2-17.5%). The differences between the two institutions in the prevalence of serologic markers for hepatitis A and B, and in the annual seroconversion rate to HBV markers reflected different rates of horizontal transmission.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Late seroconversion to hepatitis B in a Somali village indicates the important role of venereal transmission.

Hepatitis B virus (HBV) markers were investigated in a cross-sectional study in 1985 on sera from 84% of the 648 inhabitants in a rural Somali village. The prevalence of HBV markers increased with age, from 9.7% in subjects less than 12 years old, to 38% in the age group 12-19 years, and to 68% in adults. HBV markers were more common in boys less than 12 years old, 13%, than in girls of the same age group, 5.8% (P less than 0.05). A rapid increase of HBV markers started at adolescence in both sexes. The female cohort showed their highest seroconversion rate during their second decade of life, while the male cohort seroconverted more rapidly in the third decade. Thus, an initially more rapid seroconversion among boys was reversed when the females reached reproductive age, and no sex difference in marker frequencies was observed in the age group 12-19 years. There was a steady increase of HBV markers during the reproductive years in both sexes. The frequencies of HBsAg, as well as total markers, were significantly higher in adult males than females, 14 vs 5.6%, and 77 vs 62%, respectively. HBV markers were more frequent in wives of HBV positive husbands than in those married to HBV negative husbands. No increased marker prevalence was observed among siblings of HBV positive children, nor among their mothers, which disproved the role of vertical and early horizontal transmission. In 1989 the four-year rate of seroconversion was investigated in villagers who were seronegative in 1985. On testing 158 sera from 319 individuals, the seroconversion rate was significantly lower among those younger than 12 years in 1985 compared to those in the older age group, 5 vs 17%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

IgG subclasses in circulating immune complexes with hepatitis B e antigen in chronic hepatitis B.

IgG subclasses of antibodies to hepatitis B e antigen (anti-HBe) complexed to HBeAg were determined in 126 HBsAg-positive sera. In the assay HBeAg complexes were bound to microtitre plates by monoclonal anti-HBe and indicated by biotinylated monoclonals to each of the four human IgG subclasses. To evaluate the specificity of the complexed IgG, serum dilutions were also tested for HBeAg and for subclasses of anti-HBe IgG. Two groups of sera were investigated: (i) 64 sera from 64 HBsAg carriers; and (ii) 62 sera from 13 HBeAg-positive patients, of whom five seroconverted to anti-HBe. At least four sera were available from each of these patients. Complexed anti-HBe IgG was detected in 22 of 30 HBeAg-positive, and in three of HBeAg-negative carrier sera. There was no significant association between presence of complexed anti-HBe and levels of HBeAg in these sera. Complexes with multiple subclass composition were found in 13 of the 25 sera with complexed anti-HBe. The most common IgG subclasses found complexed to HBeAg were IgG1 (75%) and IgG4 (67%). A significant association (P less than 0.05) was found between the presence of free and complexed anti-HBe IgG1 in the carrier sera, indicating that the IgG1 antibodies, complexed to HBeAg, were specific for HBeAg. In the five patients who seroconverted to anti-HBe, anti-HBe IgG1 was detected in the HBeAg-positive phase before seroconversion. In the eight patients with persistent HBeAg antigenemia, free anti-HBe IgG1 was detected in only two sera from two different patients. In one patient, complexed anti-HBe IgG1/IgG4 was detected in all serum samples drawn during a period of 111 months. In conclusion, complexed anti-HBe might be detected several years before apparent seroconversion to anti-HBe in conventional anti-HBe assays. In contrast 'free' anti-HBe IgG1, when detected in HBeAg-positive sera with our anti-HBe subclass assay, seemed to signal ensuing apparent seroconversion to anti-HBe.

Adult↗

PubMed1990

Comparison of class and subclass distribution of antibodies to the hepatitis B core and B e antigens in chronic hepatitis B.

The IgG subclasses IgM and IgA1 of antibodies to hepatitis B core antigen (anti-HBc) and hepatitis B e antigen (anti-HBe) were assayed in sera from 82 patients with chronic hepatitis B utilising class/subclass-specific enzyme immunoassays (EIA). The solid-phase was either recombinant hepatitis B core antigen (rHBcAg) or rHBcAg converted to HBeAg by addition of 0.1% SDS with remaining HBcAg antigenicity blocked with monoclonal anti-HBc. Anti-HBc IgG1 was detected in 81 sera at a geometrical mean titre (GMT) of 296,110 x divided by 2.9. Anti-HBc IgG2 was not detected in any of the sera, and anti-HBc IgG3 and IgG4 were detected in 50 and 37 sera, respectively. Anti-HBc IgM and IgA1 were both significantly correlated to the presence of HBV DNA. The predominant antibody to HBeAg was found to be IgG1, being detected in 45 sera with a GMT of 1,035 x divided by 3.3. Anti-HBe IgG2 was not detected in any serum, while anti-HBe IgG3 and IgG4 were found in 8 and 23 sera, respectively. Anti-HBe IgG1, IgG3, and IgG4 were mainly detected in sera positive for anti-HBe in RIA (Abbott). No patient was found positive for anti-HBe IgA1 or IgM. Thus, in contrast to HBcAg, HBeAg does not trigger a persistent IgM and IgA1 response in chronic hepatitis B. The levels of anti-HBe IgG1 and IgG3 were much lower than the levels of anti-HBc IgG1 and IgG3. The presence of anti-HBe IgG4 was significantly correlated to that of anti-HBc IgG4.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗