<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sedohara A</submitter><funding>The University of Tokyo</funding><funding>the Ministry of Education, Culture, Sports, Science, and Technology of Japan.</funding><pagination>103</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11023964</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>169(5)</volume><pubmed_abstract>Missense mutations in certain small envelope proteins diminish the efficacy of antibodies. Consequently, tracking the incidence and types of vaccine-escape mutations (VEMs) was crucial both before and after the introduction of universal hepatitis B vaccination in Japan in 2016. In this study, we isolated hepatitis B virus (HBV) DNA from 58 of 169 hepatitis B surface antigen (HBsAg)-positive blood samples from Japanese blood donors and determined the nucleotide sequence encoding the small envelope protein. DNA from six (10%) of the samples had VEMs, but no missense mutations, such as G145R, were detected. Complete HBV genome sequences were obtained from 29 of the 58 samples; the viral genotype was A1 in one (3%), A2 in three (10%), B1 in nine (31%), B2 in five (17%), B4 in one (3%), and C2 in 10 (34%) samples. Tenofovir-resistance mutations were detected in two (7%) samples. In addition, several core promoter mutations, such as 1762A>T and 1764G>A, and a precore nonsense mutation, 1986G>A, which are risk factors for HBV-related chronic liver disease, were detected. These findings provide a baseline for future research and highlight the importance of ongoing monitoring of VEMs and drug resistance mutations in HBV DNA from HBsAg-positive blood donors without HBV antibodies.</pubmed_abstract><journal>Archives of virology</journal><pubmed_title>Characterization of mutations in hepatitis B virus DNA isolated from Japanese HBsAg-positive blood donors in 2021 and 2022.</pubmed_title><pmcid>PMC11023964</pmcid><funding_grant_id>000000</funding_grant_id><pubmed_authors>Tsutsumi T</pubmed_authors><pubmed_authors>Yotsuyanagi H</pubmed_authors><pubmed_authors>Tuvshinjargal K</pubmed_authors><pubmed_authors>Sedohara A</pubmed_authors><pubmed_authors>Arizono K</pubmed_authors><pubmed_authors>Saito M</pubmed_authors><pubmed_authors>Arai K</pubmed_authors><pubmed_authors>Nakahara F</pubmed_authors><pubmed_authors>Ikeuchi K</pubmed_authors><pubmed_authors>Takahashi K</pubmed_authors><pubmed_authors>Adachi E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Characterization of mutations in hepatitis B virus DNA isolated from Japanese HBsAg-positive blood donors in 2021 and 2022.</name><description>Missense mutations in certain small envelope proteins diminish the efficacy of antibodies. Consequently, tracking the incidence and types of vaccine-escape mutations (VEMs) was crucial both before and after the introduction of universal hepatitis B vaccination in Japan in 2016. In this study, we isolated hepatitis B virus (HBV) DNA from 58 of 169 hepatitis B surface antigen (HBsAg)-positive blood samples from Japanese blood donors and determined the nucleotide sequence encoding the small envelope protein. DNA from six (10%) of the samples had VEMs, but no missense mutations, such as G145R, were detected. Complete HBV genome sequences were obtained from 29 of the 58 samples; the viral genotype was A1 in one (3%), A2 in three (10%), B1 in nine (31%), B2 in five (17%), B4 in one (3%), and C2 in 10 (34%) samples. Tenofovir-resistance mutations were detected in two (7%) samples. In addition, several core promoter mutations, such as 1762A>T and 1764G>A, and a precore nonsense mutation, 1986G>A, which are risk factors for HBV-related chronic liver disease, were detected. These findings provide a baseline for future research and highlight the importance of ongoing monitoring of VEMs and drug resistance mutations in HBV DNA from HBsAg-positive blood donors without HBV antibodies.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-05-19T03:18:59.574Z</modification><creation>2026-05-19T03:07:27.95Z</creation></dates><accession>S-EPMC11023964</accession><cross_references><pubmed>38632180</pubmed><doi>10.1007/s00705-024-06016-4</doi></cross_references></HashMap>