Hepatitis B virus sequence changes evolving in liver transplant recipients with fulminant hepatitis
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Cited by (53)
Detecting exact breakpoints of deletions with diversity in hepatitis B viral genomic DNA from next-generation sequencing data
2017, MethodsCitation Excerpt :Hepadnaviridae show higher evolution rates than other DNA viridae and human genomes but lower rates than RNA viridae. The evolution rates of HBV have been calculated to be in the ranges of 1–5 × 10−5 and 5–8 × 10−5 per site per year in immuno-competent patients [7], 6–18 × 10−3 in liver transplant recipients with fulminant reinfection [8], and 0.3–1.3 × 10−3 for the HBV core gene in a case of perinatally acquired chronic HBV infection [9]. More than 1011 HBV virions can be produced daily in a single patient [10].
Hepatitis B virus PreS/S gene variants: Pathobiology and clinical implications
2014, Journal of HepatologyCitation Excerpt :The infecting viruses were genetically almost identical in both patients and carried a double nucleotide mutation in the start codon of the preS2 region that prevented the synthesis of the corresponding protein, as also confirmed by immunoassay experiments (of note, the virus isolates from both patients had wild-type preCore and BCP sequences in the early phases of the infections) [10]. Moreover, we detected preS2-defective mutants in additional cases of FH and similar findings were subsequently reported by other authors [102,103]. Although experimental studies definitively confirming the suspected role of preS2-defective HBV in the pathogenesis of the acute liver failure are still lacking, it is noteworthy to mention that intracellular retention of HBV surface proteins was found to be associated with FH in a transgenic mouse model showing panlobular necrosis and hepatic failure as a consequence of the extreme sensitivity of hepatocytes with HBV surface protein retention to interferon-gamma produced by the cytotoxic T lymphocytes [104].
Molecular Biology of the Hepatitis B Virus for Clinicians
2012, Journal of Clinical and Experimental HepatologyCitation Excerpt :However, the rate of evolution and emergence of variants may greatly differ in different clinical settings, depending upon the pressure exerted by the host immune system, vaccine immunophophylaxis or antiviral drugs. It has been reported that mutation rate is almost 100-fold higher in immune-suppressed patients as compared to subjects having silent or occult HBV infection.82,83 Nevertheless as a result of complex host–virus interactions, mutations emerging under different types of selective pressure are either fixed in the genome if advantageous or eliminated during subsequent cycles if disadvantageous.
Determination of hepatitis B virus genotype by flow-through reverse dot blot
2007, Journal of Clinical VirologyCitation Excerpt :Some of these techniques are commercially available, but most are relatively time consuming, labor intensive, costly and sensitive to single nucleotide mutations (Bartholomeusz and Schaefer, 2004). Since mutations accumulate at a rate of 1.4–3.2 × 10−5 nucleotide substitutions per site per year (Okamoto et al., 1987) and even more rapidly in liver transplant patients (Sterneck et al., 1997), a method insensitive to a single nucleotide mutation within genotype specific sequences might be a clinical advantage. A flow-through form of the reverse dot blot (RDB) assay (FT-RDB) described in our laboratory is rapid and inexpensive (Ou et al., 2005).
Genetic variability of the S gene of hepatitis B virus: Clinical and diagnostic impact
2005, Journal of Clinical Virology