Our results show that combined active-passive immunization of newborns against hepatitis B provides persistent protection up to adolescence despite a frequent waning of anti-HBs antibodies, suggesting there is no need for booster vaccination during adolescence.
Perinatal transmission of and infection with hepatitis B (HBV) in early childhood are observed in a small proportion of the offspring of hepatitis B surface antigen (HBsAg)-positive mothers who are vaccinated against HBV immediately after giving birth. The children may be infected by wild-type HBV or by variants with amino acid substitutions in the "a" determinant of HBsAg, particularly at position 145 and, rarely, at positions 120, 126, 129, 131, 141, and 144. Four hundred and forty-six newborn infants of HBsAg-positive mothers in the northeastern part of the Czech Republic received combined active and passive immunisation against HBV. Only one child became an HBsAg carrier. This followed a mild, acute HBV illness in the beginning of the second year of his life. HBV DNA encoding the "a" determinant and surrounding region of HBsAg was sequenced after amplification from the plasma of the child and his mother. The child was infected with variants of HBsAg with substitutions at residues 137 and 139. The virus of the mother had changes at residues 120 and 121. HBV from both child and mother had an unusual substitution at residue 118 and seemed to be of the ayw subdeterminant.
Patients with renal insufficiency are at high risk of contracting hepatitis B virus (HBV) infection during dialysis. 1 Despite routine vaccination and other preventive measures to protect such patients against HBV infection, 2-4 outbreaks continue to be reported in dialysis units. 5,6 Conventional HBV vaccines are weakly immunogenic in patients with renal insufficiency, with Background: three doses of the investigational aS02 v -adjuvanted hepatitis B virus (HBV) vaccine HB-aS02 have been shown to induce more rapid seroprotection and higher anti-HBs antibody concentrations in patients with renal insufficiency than four doses of FENDrix tM (HB-aS04), an adjuvanted HBV vaccine licensed in europe for use in this population. this study evaluated persistence of immune response up to 36 mo after primary vaccination.Results: at Month 36, 89.5% of subjects in the HB-aS02 group and 72.6% of those in the HB-aS04 group had antiHBs antibody concentrations ≥10 mIU/ml. anti-HBs antibody concentrations were ≥100 mIU/ml in 82.9% and 35.5% of subjects, respectively. anti-HBs geometric mean antibody concentrations were higher in the HB-aS02 group over the 36 mo of follow-up. an exploratory "time to boost" analysis confirmed that subjects who received HB-aS02 were 2.54 times more likely than those who received HB-aS04 to have anti-HBs antibody concentrations ≥10 mIU/ml at Month 36 (p = 0.013).Methods: In this open, international, phase III follow-up study, 151 pre-dialysis, peritoneal dialysis and hemodialysis patients ≥15 y of age received HB-aS02 at 0, 1 and 6 mo and 149 received HB-aS04 at 0, 1, 2 and 6 mo. of these, 99 and 80 returned at Month 36, 76 and 62 of whom were eligible for inclusion in the long-term according-to-protocol (Lt-atp) cohort for descriptive analysis of antibody persistence (mean age: 65.6 y).conclusion: HB-aS02 candidate vaccine induces high and persistent anti-HBs antibody levels in pre-dialysis, peritoneal dialysis and hemodialysis patients, potentially reducing the need for booster doses in this population.
Hepatitis C virus (HCV) is a single-stranded positive-sense RNA virus from the genus Hepacivirus. The viral genomic +RNA is 9.6 kb long and contains highly structured 5′ and 3′ untranslated regions (UTRs) and codes for a single large polyprotein, which is co- and post-translationally processed by viral and cellular proteases into at least 11 different polypeptides. Most of the 5′ UTR and an initial part of the polyprotein gene are occupied by an internal ribosome entry site (IRES), which mediates cap-independent translation of the viral proteins and allows the virus to overcome cellular antiviral defense based on the overall reduction of the cap-dependent translation initiation. We reconsidered published results concerning a search for possible correlation between patient response to interferon-based antiviral therapy and accumulation of nucleotide changes within the HCV IRES. However, we were unable to identify any such correlation. Rather than searching for individual mutations, we suggest to focus on determination of individual and collective activities of the HCV IRESs found in patient specimens. We developed a combined, fast, and undemanding approach based on high-throughput cloning of the HCV IRES species to a bicistronic plasmid followed by determination of the HCV IRES activity by flow cytometry. This approach can be adjusted for measurement of the individual HCV IRES activity and for estimation of the aggregate ability of the whole HCV population present in the specimen to synthesize viral proteins. To detect nucleotide variations in the individual IRESs, we used denaturing gradient gel electrophoresis (DGGE) analysis that greatly improved identification and classification of HCV IRES variants in the sample. We suggest that determination of the collective activity of the majority of HCV IRES variants present in one patient specimen in a given time represents possible functional relations among variant sequences within the complex population of viral quasispecies better than bare information about their nucleotide sequences. A similar approach might be used for monitoring of sequence variations in quasispecies populations of other RNA viruses in all cases when changes in primary sequence represent changes in measurable and easily quantifiable phenotypes.
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