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Background & Aims: The aim of this study was to investigate the influence of hepatitis B virus (HBV) genotypes on the clinical outcome of chronic childhood HBV infection and hepatocellular carcinoma (HCC). Methods: A total of 460 HBV carrier children were followed-up for 15 years and 26 children with HBV-related HCC were recruited. HBV genotyping was examined at enrollment and the latest follow-up of these carrier children and at diagnosis in HCC children. Viral load was checked at enrollment for the carrier children. These carriers were grouped based on their initial hepatitis B e antigen (HBeAg) and antibody to hepatitis B e antigen (anti-HBe) status. The HBeAg positive (+) group was divided further into an HBeAg(+/+) group and HBeAg(+/-) group, depending on whether spontaneous HBeAg seroconversion occurred during the follow-up period. Results: Genotype B constituted 73%, 86%, and 76% in the HBeAg(+/+), HBeAg(+/-), and anti-HBe(+) groups, respectively. Genotype C was found in 27%, 8%, and 6% in the HBeAg(+/+), HBeAg(+/-), and anti-HBe(+) group, respectively. Genotype C carriers were more prevalent in the HBeAg(+/+) group than the other 2 groups (P = .01), and had a delayed HBeAg seroconversion compared with the genotype B carriers (P < .001). Changes of genotype during the follow-up period were rare (2.8%). In those with HCC, genotype B was also the major type (74%). There was no difference in the baseline viral load between genotypes B and C. Conclusions: Although HBV genotype B dominates in children with chronic HBV infection and HCC in Taiwan, genotype C delays HBeAg seroconversion in pediatric chronic HBV infection.

Studies were conducted to investigate the impact of a selected lactobacilli mixed culture on Campylobacter jejuniin simulated chicken digestive tract models. Veronal buffer solutions corresponding to the pH of successive segments of the chicken digestive tract were prepared. The lactobacilli mixtures were prepared by mixing four fresh lactobacilli cultures, including Lactobacillus acidophilus, Lactobacillus fermentum, Lactobacillus crispatus, and Lactobacillus brevis. The C. jejuniand lactobacilli mixture were mixed with sterile poultry feed, and the previously prepared veronal buffer solutions were then added separately. The mixture was incubated at 41.1°C for various lengths of time with periodic agitation. The feed passage time for five segments of the digestive tract were adopted: crop (pH 4.5), 30 min; proventriculus (pH 4.4), 15 min; gizzard (pH 2.6), 90 min; small intestine (pH 6.2), 90 min; and large intestine (pH 6.3), 15 min. The Campylobacterand lactobacilli were enumerated. An antagonistic effect on C. jejuniby the tested lactobacilli spp. was found in individual sections and the complete simulated digestive tract models. In the simulated complete chicken digestion system, no C. jejuniwere found during the final incubation period when a lactobacilli mixture was present. The results of this in vitro study indicate the potential value of future in vivo studies.

Objectives: To study viral persistence and antibody responses after hepatitis G virus (HGV) infection in children of various ages. Study design: We performed an enzyme immunoassay for antibodies to E2 protein (anti-E2) of HGV and reverse-transcription polymerase chain reaction assay for HGV RNA on serum samples. Results: Of 28 infants born to HGV RNA-positive mothers, 17 were found to be positive for HGV RNA. None were positive for anti-E2. All 17 infected infants continued to have viremia except 1 who converted to HGV RNA-negative status at 24 months. Six infants had mild elevations of alanine aminotransferase levels (5 HGV-positive and 1 HGV-negative). An additional 14 HGV-infected children (aged 6 months to 14 years) with posttransfusion HGV infection were tested for anti-E2 3 months and 12 months after blood transfusion. None of the HGV RNA-positive serum samples were positive for anti-E2; however, 4 of the 8 children with resolving HGV infection were positive for anti-E2 1 year later. Conclusions: Mother-to-infant transmission of HGV resulted in a high viral persistence rate and lack of immune responses to HGV. In contrast, anti-E2 appeared in children who recovered from posttransfusion HGV infection. Mode of transmission and age at infection may be important factors in determining persistent HGV infection and defective immune response to HGV. (J Pediatr 1998;133:382-5)

Objective: To investigate the prevalence and outcome of hepatitis B surface antigenemia in newborns of hepatitis B e antigen (HBeAg)-positive hepatitis B surface antigen (HBsAg) carrier mothers under the current immunoprophylaxis program. Study design: From 1984 to 1993, 665 high-risk newborns born to HBeAg-positive HBsAg carrier mothers were prospectively recruited. The newborns were tested for HBsAg soon after birth, before hepatitis B immune globulin administration. All newborns received hepatitis B immune globulin within 24 hours after birth plus subsequent hepatitis B vaccination. Those who were seropositive for HBsAg at birth were regularly followed up for their hepatitis B virus (HBV) markers, liver function profiles, and @a-fetoprotein levels from 1984 to 1996. Results: Sixteen (2.4%) of the 665 subjects were found to be seropositive for HBsAg at birth, and all remained HBsAg-positive at 6 months of age. Twelve of the 16 received long-term follow-up care, and all were confirmed to have chronic HBV infection. Of the 12, 2 had HBeAg seroconversion, and 1 had alanine aminotransferase flares without HBeAg seroconversion. Delayed appearance of hepatitis B core antibody (anti-HBc) occurred in 2 without alanine aminotransferase elevation. Conclusions: Current immunoprophylaxis strategy does not protect newborns with surface antigenemia, apparently acquired in utero, from becoming HBV carriers. Immunologic attempts to eliminate HBV may occur in carrier children infected in utero, despite their profound immune tolerance to HBV. (J Pediatr 1998;133:374-7)

Objective: To investigate the safety, immunogenicity, and efficacy of a simplified hepatitis B vaccination schedule. Methods: The second dose of hepatitis B vaccine and the first dose of diphtheria-tetanus-pertussis (DTP) vaccine were given simultaneously at age 6 weeks. The second dose of DTP vaccine was given at age 3.5 months. The third dose of DTP vaccine and the third dose of hepatitis B vaccine were given at age 5.5 months. One hundred three infants (group A) born to mothers without hepatitis B surface antigen (HBsAg) received DTP with whole-cell pertussis vaccine. Fifty-five infants (group B) born to mothers with HBsAg and hepatitis B e antigen received DTP with acellular pertussis vaccine. Results: By age 9 months, none of group A and 4 (7%) group B infants were seropositive for HBsAg. The protective efficacy against the hepatitis B carrier state in these infants at high risk was 92%. Antibody to hepatitis B surface antigen was 10 mIU/ml or greater in 99 (96%) of group A infants and in 50 (91%) of group B infants. Both the acellular and whole-cell DTP vaccines were immunogenic, and the incidences of adverse reactions were within an expected and acceptable range. Conclusions: The simplified vaccination schedule to integrate the hepatitis B vaccine into the Expanded Programme of Immunization was safe, immunogenic, and effective. This schedule may improve vaccine compliance and be applied to DTP and hepatitis B combination vaccines now under investigation. (J Pediatr 1997;130:981-6)

Objectives: To delineate the importance of non-A, non-B, non-C (non-ABC) hepatitis, and the role of GB virus C (GBV-C) in children. Methods: From 1980 to 1995, acute-onset viral hepatitis was diagnosed in 166 inpatients and categorized into type A, B, C, and non-ABC hepatitis according to the serologic markers or the results of polymerase chain reaction assay for HBV DNA or HCV ribonucleic acid (RNA) in the National Taiwan University Hospital. Non-ABC hepatitis was diagnosed in 57 patients (34%). GBV-C RNA was investigated by reverse transcription and nested polymerase chain reaction in 32 of the 57 patients with non-ABC hepatitis. The clinical and laboratory features of patients with acute non-ABC hepatitis were compared with the features of those with acute hepatitis A and B. Results: The degree of abnormality in aminotransferase activities was milder in patients with non-ABC hepatitis than in those with hepatitis B; chronicity was noted in 12%. Fulminant hepatitis occurred in 16%, and the mortality rate was 56%. Young age carried a significantly higher risk of having a fulminant course (1.9 +/- 0.2 years of age vs 6.4 +/- 5.1 years of age in acute course; p < 0.05). Compared with fulminant hepatitis B, fulminant non-ABC hepatitis had a trend of a longer interval from onset to death (119.2 +/- 144.8 vs 15.2 +/- 8.4 days; p = 0.079). GBV-C RNA was detected in only two of the patients tested, both of whom had received transfusions; one had persistent viremia and fluctuating aminotransferase values. Conclusions: Non-ABC hepatitis plays an important role in the etiology of pediatric viral hepatitis; however, the role of GBV-C is minor. A search for other unknown viral agent(s) responsible for non-ABCG hepatitis is needed. (J Pediatr 1997;131:536-40)