Virusliterature

HBV mutation literature information.

Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies.

PMID: 32532295 2020 Virology journal

Abstract: Clinical prognosis-related genetic variations such as nucleotide mutation T1762/A1764 (27.93%), A2189C (12.85%), G1613A (8.94%), T1753C (8.38%), T53C (4.47%) T3098C (1.68%) and PreS deletion (2.23%) were detected in CD recombinants.

Table:

Table: A1516C

Table: A1762T

Spontaneous reactivation of hepatitis B virus with S gene mutations in an elderly patient with diabetic nephropathy.

PMID: 32519312 2020 Clinical journal of gastroenterology

1Abstract: Full-genome HBV sequence analysis revealed that the patient was infected with HBV of subgenotype B1 and it had an ""a"" determinant mutation M133L in the S gene coding HBsAg."

Entecavir-resistant hepatitis B virus decreases surface antigenicity: A full genome and functional characterization.

PMID: 32216026 2020 Liver international

Abstract: Additionally, the ETV resistance mutations rtT184A/L, rtS202G and rtM250V were found among three patients.

Abstract: More importantly, the rtI169T mutation in the RT domain, led to the sF161L mutation in the overlapping S gene, which decreased in surface antigenicity.

Abstract: RESULTS: The rtL180M + rtM204V mutations were common among all the clones analysed.

Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection.

PMID: 33458253 2020 Wellcome open research

Abstract: Through application of deep whole-genome sequencing we typed the isolate as genotype-D1, and identified several minority variants including G1764A and G1986A substitutions in the pre-core promoter and pre-core regions, which support CHB-AR rather than AHB.

Table: A128V

Table: A1762T

Structural features in common of HBV and HIV-1 resistance against chirally-distinct nucleoside analogues entecavir and lamivudine.

PMID: 32080249 2020 Scientific reports

Abstract: Additionally, we experimentally simulated previously reported ETV/3TC resistance for HBV using HIVY115F/F116Y/Q151M with F160M/M184V (L180M/M204V in HBV RT) substituted.

Introduction: 3TC is also approved as an anti-HIV-1 agent, and M184V in HIV-1 RT, which corresponds to M204V in HBV RT, has also been reported as an amino acid substitution responsible for 3TC resistance in HIV-1.

Introduction: Accordingly, we assumed that crystallographic studies of HIV-1 RT containing HBV-associated amino acids at the N-site should also provide important clues for understanding the mechanism of 3TC/ETV resistance caused by common M204V/I in HBV RT (M184V/I in HIV-1

7-Deaza-7-fluoro modification confers on 4'-cyano-nucleosides potent activity against entecavir/adefovir-resistant HBV variants and favorable safety.

PMID: 32084506 2020 Antiviral research

Abstract: Southern blot analysis using wild-type HBV (HBVWT)-encoding-plasmid-transfected HepG2 cells revealed that CdFA efficiently suppresses the production of HBVWT (IC50 = 153.7 nM), entecavir (ETV)-resistant HBV carrying L180M/S202G/M204V substitutions (HBVETVR; IC50 = 373.2 nM), and adefovir dipivoxil (ADV)-resistant HBV carrying A181T/N236T substitutions (HBVADVR; IC50=192.6 nM), whereas ETV and ADV were less potent against HBVETVR and HBVADVR (IC50: >1,000 and 4,02

Result: We then analyzed the interactions of ETV-TP and CdFA-TP with HBV-RT, in which three amino acid substitutions associated with HBV's resistance to ETV (L180M/S202G/M204V) have been introduced (RTETV-R).

A Hyper-Glycosylation of HBV Surface Antigen Correlates with HBsAg-Negativity at Immunosuppression-Driven HBV Reactivation in Vivo and Hinders HBsAg Recognition in Vitro.

PMID: 32102257 2020 Viruses

Abstract: These NLGSs are located in the major hydrophilic region of HBsAg (known to be the target of antibodies) and resulted from the single mutation T115N, T117N, T123N, N114ins, and from the triple mutant S113N+T131N+M133T.

Discussion: Considering the N-linked glycosylation sites observed in our study, recent studies have shown that the mutational profile T131N+M133T reduces HBsAg antigenicity and fails to induce anti-HBs response without altering HBV replicative capacity.

Discussion: Furthermore, another study has shown that the N-linked glycosylation site

[The prevalence clinically significant virus mutations among patients with chronic viral hepatitis B.]

PMID: 32155009 2020 Klinicheskaia laboratornaia diagnostika

Abstract: Another 12.5% of the isolates are characterized by mutations that are independently associated with the liver cirrhosis and hepatocellular carcinoma development, including 21, 24, 27 nucleotides deletions in the Pre-S2 region and the S11F mutation in the PreCore region.

Key mutations in the C-terminus of the HBV surface glycoprotein correlate with lower HBsAg levels in vivo, hinder HBsAg secretion in vitro and reduce HBsAg structural stability in the setting of HBeAg-negative chronic HBV genotype-D infection.

PMID: 32312174 2020 Emerging microbes & infections

Abstract: Results confirmed by multivariable analysis correcting for patients'demographics, HBV-DNA, ALT and infection-status.In genotype-D, specific C-terminus mutations (V190A-S204N-Y206C-Y206F-S210N) significantly correlate with HBsAg<1000IU/ml(P-value from <0.001 to 0.04).

Abstract: These mutations lie in divergent pathways involving other HBsAg C-terminus mutations: V190A + F220L (Phi = 0.41, P = 0.003), S204N + L205P (Phi = 0.36, P = 0.005), Y206F + S210R (Phi = 0.47, P < 0.001) and S210N +

Anti-HBV activity of the HBV capsid assembly modulator JNJ-56136379 across full-length genotype A-H clinical isolates and core site-directed mutants in vitro.

PMID: 32417895 2020 The Journal of antimicrobial chemotherapy

Abstract: Core amino acid substitutions in the CAM-binding pocket, when tested as SDMs at positions 23, 25, 30, 33, 37, 106, 110, 118, 124, 127 and 128, reduced JNJ-56136379 anti-HBV activity; EC50 fold increases ranged from 3.0 (S106T) to 85 (T33N).

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