Surface gene mutations of hepatitis B virus among high-risk patients with occult hepatitis B virus infection

T cell responses and viral variability in blood donation candidates with occult hepatitis B infection

“…The G145R mutation (vaccine escape mutation) and cysteine substitutions in positions 121, 124, 137, or 147 are the most destructive mutations on HBsAg conformation and epitope structure [41,42]. Amino acid substitutions at codons 116 and 118 or a translational stop codon at positions 69, 199, or 216 have also led to failure of HBsAg detection [39]. In contrast to some studies [39], our OBI donors presented a high mutation rate in the ''a'' determinant, which suggests an altered HBV humoral response as has been previously suggested [18,19,29], or the possibility that mutations in the ''a'' determinant play a major role in HBsAg detection.…”

“…Amino acid substitutions at codons 116 and 118 or a translational stop codon at positions 69, 199, or 216 have also led to failure of HBsAg detection [39]. In contrast to some studies [39], our OBI donors presented a high mutation rate in the ''a'' determinant, which suggests an altered HBV humoral response as has been previously suggested [18,19,29], or the possibility that mutations in the ''a'' determinant play a major role in HBsAg detection. However, no mutations leading to stop codons were found.…”

“…Nevertheless, we observed a high amino acid mutation rate and strong selective pressure acting on HBsAg protein and especially on the MHR of OBI donors, and this selective pressure could be induced by T cell immune responses. Mutations in the HBV surface gene have been reported in various patient groups [2,21,39], and HBV mutations interfere with viral replication and antibody recognition of HBsAg [39][40][41][42]. Most of these mutations affect the ''a'' determinant (aa 124-147), which is essential for epitope presentation and assay reactivity.…”

Occult Hepatitis B Virus Infection in Anti-HBs-Positive Infants Born to HBsAg-Positive Mothers in China

“…The occult status of infection may be due to host immunosuppression, co-infection with hepatitis C virus (HCV), the window period after acute infection, genetic mutations in the S gene, or other host factors [11],13],[14]. The clinical consequence and transmission risk of OBI in populations remains unclear.…”

Absence of occult hepatitis B virus infection in sera of diabetic children and adolescents following hepatitis B vaccination

“…4 The occult status of infection in vaccinated children may be a result of host immunosuppression, genetic mutation of the S gene, transmission to children from occultinfected or HBsAg-positive mothers, or other host factors. [5][6][7] OBI may persist in individuals for years without obvious symptoms of HBV infection, 8 or it may progress to hepatitis, liver cirrhosis, and/or hepatocellular carcinoma. 7 The incidence of OBI in HB-vaccinated children varies in groups with different risk factors and according to geographic location in concordance with the local incidence of HBV, irrespective of antibody to HBsAg (anti-HBs) serostatus.…”