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Hepatitis B virus S gene mutants in infants infected despite immunoprophylaxis
1Department of Infectious Diseases, Children's Hospital, Medical Center of Fudan University, Shanghai 200032, China.
Insights
Hepatitis B virus (HBV) surface gene mutations are prevalent in infants experiencing vaccination failure. These HBV mutants can be transmitted from mothers to infants, contributing to immunoprophylaxis failure.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Hepatitis B virus (HBV) infection remains a significant global health concern.
- Hepatitis B (HB) vaccination is a primary strategy for preventing HBV infection.
- Vaccination failure can occur, necessitating further investigation into underlying causes.
Purpose of the Study:
- To investigate the correlation between hepatitis B virus (HBV) surface gene mutant infections and the failure of hepatitis B (HB) vaccination.
- To identify specific HBV S gene mutations associated with vaccination failure in infants born to HBV carrier mothers.
Main Methods:
- Sera from 106 infants with failed HB immunoprophylaxis were analyzed.
- HBV S gene was amplified using PCR, followed by Southern blot hybridization with oligonucleotide probes.
- DNA sequencing was performed on non-hybridizing samples to confirm mutations.
Main Results:
- 93.4% of infants tested positive for HBV DNA.
- 30.3% of these samples showed mutations in the HBV S gene, failing to hybridize with specific probes.
- DNA sequencing identified mutations in 10 out of 11 tested samples, including amino acid changes at various positions.
Conclusions:
- Approximately 30% of infants experiencing HB vaccination failure harbor HBV surface mutants.
- These identified HBV mutants are capable of infecting infants through maternal-infant transmission.
- The findings highlight the role of HBV mutants in vaccine escape and vertical transmission.
Objective:
To assess the correlation between hepatitis B virus (HBV) surface gene mutant infection and hepatitis B (HB) vaccination failure.
Methods:
Using sera from 106 infants who were born to HBV carrier mothers and failed in HB immunoprophylaxis, HBV S gene was amplified by PCR, transferred to nylon membranes for Southern blots, and then hybridized with oligonucleotide probes. Eleven of non-hybridizing samples were used for DNA sequencing.
Results:
93.4% (99/106) of the samples were HBV DNA positive, and 30.3% (30/99) failed to hybridize with at least one of the four probes. DNA sequencing confirmed that 10 of the 11 samples had an S gene mutation with amino acid (aa) change. The identified mutants included nucleotide (nt) 546T-->A (aa131N-->T), nt531T-->C (aa1261-->T), nt491A-->C (aa113T-->P), nt491T-->A (aa113S-->T), nt533C-->A (aa127P-->T), nt581T-->A (aa143S-->T), nt636A-->T (aa161Y-->F), and nt679A-->C (aa175L-->F). The sequence in one mother-infant pair was completely the same, with mutations at aa131 and aa161.
Conclusions:
The prevalence of HBV surface mutants is about 30% in the children failing in HB vaccination. HBV mutants can infect infants by maternal-infant transmission.