The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV

He, Lingyuan; Su, Mingze; Ou, Guomin; Wang, Luwei; Deng, Juan; Zhang, Hui; Xiang, Kuanhui; Li, Tong

doi:10.1016/j.meegid.2019.104006

Cited by 2 publications

(1 citation statement)

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“…It is worth noting that the AGL sequences of the GTB and GTC differ at least by three AAs (GTB/GTC: sT/I126, sT/S143 and sK/R160), which are genotype-dependent polymorphic AA sites. The sK/R160 is known as a HBV serotype related AA site, whereas the mutations at s126 site have been extensively studied and shown to affect HBV secretion or HBsAg antigenicity [ 32 ]. Whether they have any effect on the glycosylation of SHBs remains uncovered.…”

Section: Discussionmentioning

confidence: 99%

Host sex disparity and viral genotype dependence of the glycosylation level of small Hepatitis B surface protein in patients with HBeAg-positive chronic Hepatitis B

Zhao

Deng

et al. 2023

Virol J

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Background Hepatitis B surface antigen (HBsAg) consists of six components of large/middle/small HBs proteins (L/M/SHBs) with non-glycosylated (ng)- or glycosylated (g)- isomers at sN146 in their shared S domain. g-SHBs plays a crucial role in hepatitis B virus (HBV) secretion. However, the host and viral factors impacting sN146 status in natural HBV infection remain revealed mainly due to the technical difficulty in quantifying g-SHBs and ng-SHBs in serum samples. Methods To establish a standardized Western blot (WB) assay (WB-HBs) for quantifying the SHBs isomers in serum samples of 328 untreated hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) patients with genotype B or C HBV infection. The 1.3-mer HBV genotype B or C plasmids were transiently transfected into HepG2 cells for in vitro study. Results The median level of ng-SHBs was significantly higher than that of g-SHBs (N = 328) (2.6 vs. 2.0 log10, P < 0.0001). The median g-/ng-SHBs ratio in female patients (N = 75) was significantly higher than that of male patients (N = 253) (0.35 vs. 0.31, P < 0.01) and the median g-/ng-SHBs ratio in genotype C patients (N = 203) was significantly higher than that of the genotype B patients (N = 125) (0.33 vs. 0.29, P < 0.0001). Conclusions Our findings suggest that the g-/ng-SHBs ratio is host-sex-biased and viral genotype dependent in treatment naïve patients with HBeAg-positive chronic hepatitis B, which indicates the glycosylation of SHBs could be regulated by both host and viral factors. The change of ratio may reflect the fitness of HBV in patients, which deserves further investigation in a variety of cohorts such as patients with interferon or nucleos(t)ide analogues treatment.

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Section: Discussionmentioning

confidence: 99%

Host sex disparity and viral genotype dependence of the glycosylation level of small Hepatitis B surface protein in patients with HBeAg-positive chronic Hepatitis B

Zhao

Deng

et al. 2023

Virol J

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Evolution of hepatitis B virus polymerase and surface genes in patients receiving finite antiviral therapy

Chu,

Hsu,

et al. 2024

J of Gastro and Hepatol

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Background and AimHepatitis B virus (HBV) reactivation could develop after withdrawal following a finite course of nucleoside analog (NA) therapy, leading to virological and clinical relapses. The genetic heterogeneity in the HBV surface and polymerase genes during finite NA therapy has not been carefully studied.MethodsSeven chronic HBV‐infected patients experiencing relapses following entecavir (ETV; n = 5; Patients 1 to 5) or tenofovir disoproxil fumarate (TDF; n = 2; Patients 6 and 7) withdrawal were included. Sera obtained before treatment and at relapses were retrieved and submitted for DNA extraction and amplicon‐specific deep sequencing.ResultsETV‐treated patients had a longer time‐to‐relapse than that of TDF‐treated patients (P = 0.0357). No drug‐resistance related polymerase mutation was detected during relapses, except for a low percentage (1.4%) of rtM204I mutation in Patient 1. Two surface truncation mutations (sW216*; 40.9% and sW182*; 4.7%) detected before treatment in two TDF‐treated patients (Patients 6 and 7, respectively) were overtaken by the wild types during subsequent drug‐withdrawal‐related relapses. The simultaneous presence of sG44E (T‐cell epitope) and sE164G (B‐cell epitope) mutations was associated with failure of HBV e antigen (HBeAg) seroclearance in ETV‐treated patients.ConclusionsIn conclusion, HBV genome continues to evolve during the courses of finite antiviral therapies. Pre‐existing surface truncation mutations can be overtaken by the wild types after relapses. The sG44E/sE164G mutations are associated with failure of HBeAg seroclearance.

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The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV

Cited by 2 publications

References 42 publications

Host sex disparity and viral genotype dependence of the glycosylation level of small Hepatitis B surface protein in patients with HBeAg-positive chronic Hepatitis B

Host sex disparity and viral genotype dependence of the glycosylation level of small Hepatitis B surface protein in patients with HBeAg-positive chronic Hepatitis B

Evolution of hepatitis B virus polymerase and surface genes in patients receiving finite antiviral therapy

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