Figure: (A) Extracellular HBV DNAs were prepared directly from equal volumes of mouse sera of WT and mutant I97L injections before Southern blot analysis.
Figure: (A) IFN-alpha receptor knockout (IFNAR-/-) mice were hydrodynamically injected with 30 mug of DNA of WT or mutant I97L HBV.
Figure: (A) Liver samples were collected at 3 days or 1 week after the hydrodynamic injection of 14 mug of HBV plasmid DNAs of WT or mutant I97L.
Figure: (B) The serum HBeAg titers in mice receiving WT or I97L DNAs were determined at the indicated time points with an enzyme immunoassay (see Materials and Methods).
Figure: (C) More rapid decay of viral DNA of mutant I97L in hepatocytes was observed by hydrodynamic delivery.
Figure: (E) Detection of only slightly reduced a
Comparison of pre-S1/S2 variations of hepatitis B virus between asymptomatic carriers and cirrhotic/hepatocellular carcinoma-affected individuals.
PMID: 31501793
2019
Clinical and experimental hepatology
Abstract: Conclusions: According to the results, point mutations such as L11Q, N37S, K38R and A49V, as well as certain deletions, may be associated with HBV infection outcome, among an HBV genotype D pure population.
Abstract: The rate of critical point mutations, including L11Q, N37S and K38R, was significantly higher in the ASC group, whereas the A49V substitution rate was significantly higher in the LC/HCC group (p < 0.05).
Discussion: An L11Q point mutation was also located in the hepatocyte binding site (p10-36 in
Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains.
Result: However, mutation Q16R resulted in decreased HBsAg secretion compared to wt M88 (EC/IC ratio: 0.57 versus 1.2) whereas a significant increase in HBsAg secretion was observed in P38.II (EC/IC ratio: 31 versus 0.5).
Result: Introduction of the N146D/S/Y mutations in plasmid M88 and P38.II by SDM did not significantly alter the EC and IC HBsAg production pattern, although a slight reduction in HBsAg secretion was observed for P38.II mutants, as reflected by the decreased HBsAg EC/IC ratio compared to that of wt HBsAg (5-8 versus 17) (Figure 3).
Result: Mutants N146D/S/Y showed an expected non-glycosylated profile.
Result: Mutations
Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure.
Abstract: A mutation in C-region of HBsAg (L216*), was associated with reduced HBsAg production and secretion.
Abstract: An HBsAg mutation (L216*) was found to be more frequent in ALF patients and was associated with reduced HBsAg production and secretion.
Discussion: Amongst the detected immune escape mutations, we found the HBsAg D144E mutation in two ALF and three non-ALF patients.
Discussion: Furthermore, the sequencing of the whole HBV genome per NGS and the functional analysis of the HBsAg
Hepatitis B virus reactivation sustained by a hepatitis B virus surface antigen immune-escape mutant isolate in a patient who was hepatitis B core antibody positive during treatment with sofosbuvir and velpatasvir for hepatitis C virus infection: a case report.
PMID: 31542053
2019
Journal of medical case reports
Abstract: Sequencing analysis revealed the hepatitis B virus genotype D3 and the presence of two relevant immune-escape mutations (P120S and T126I) in the major hydrophilic region by analyzing the S region.
Conclusion: In contrast, by analyzing the S region, two relevant mutations, P120S and T126I, localized in the major hydrophilic region, an immune-active HBsAg domain, were found.
Discussion: In the first case, genome sequencing revealed a T118K mutation in the S region, but in contrast to our description, the HBV viremia occurred 5 months after the EOT with daclatasvir and asunaprevir.
Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro.
PMID: 31543688
2019
World journal of gastroenterology
Result: Among 40 patients treated with low genetic barriers, one of four patients with pre-existing rtM204I variants (1/4, 25.0%) and half of patients without pre-existing rtM204I variants (18/36, 50.0%) achieved CVR at 12 mo of low genetic barriers.
Result: Among 95 patients treated with tenofovir, all seven patients with pre-existing rtM204I variants (7/7, 100%) as well as almost patients without pre-existing rtM204I variants (85/88, 96.6%) achieved CVR at 12 mo of tenofovir.
Result: Among 97 patients treated with entecavir, only one of six patients with pre-existing rtM204I variants (1/6, 16.7%) achieved CVR at 12 mo of entecavir,
Prevalence of Hepatitis B Virus Infection in Shenzhen, China, 2015-2018.
Abstract: NAs resistant mutation occurrence patterns were multitudinous; single mutation patterns of rtM204I/V and rtL180M occurrences accounted for majority, followed by the combinational mutation pattern L180M + M204I/V.
Result: Among them, mutation rtM204I associated with LAM and LdT had the highest proportion, 38.33%; mutation rtL180M associated with LAM, LdT, and ETV accounted for 19.30%; mutation rtM204V associated with LAM, LdT, and ETV accounted for 12.97%; and other mutations accounted for no more than 10%.
Result: Combinational mutation occu
Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients.
Result: In addition to previously reported mutations, we also found five variants of the X gene located in the HBV functional region, including L37I, S43P, H86P/R, L98I and T105A, which have not been reported in previous studies and may be specific for Indonesian HBV.
Result: Multinomial regression analysis confirmed that K130M/V131I mutations were correlated with CLD progression (OR, 7.629; 95% CI, 1.578-36.884; Table V).
Result: The dominant mutations in the basal core promoter (BCP) were K130M/V131I, as found in 12.6% (11/87) of CLD patients.
High frequency of drug resistance mutations in the HBV genome in ART-experienced HIV-coinfected patients in southwestern Nigeria.
Abstract: Between compartments, core gene variants revealed Arg94Leu, Glu86Arg and Ser41Thr while X gene variants revealed Phe73Val, Ala44Val, Ser146Ala and Ser147Pro.
Abstract: In addition, a virus surface antigen mis-sense mutation resulting in M125T was detected in all the samples and could account for surface antigen negativity and occult HBV status.
Abstract: In tumor compartments per se, several mis-sense mutations were detected, notably the classic T1762A/A1764G mutation in the
ViMRT
HBV mutation literature information.
PMID: 
2019
Journal of virology
