ArticleFrontiers in cellular and infection microbiology2026
Impact of hepatitis B virus surface antigen mutations in the major hydrophilic region on antigen detectability.
Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aims to investigate the impact of mutations within the major hydrophilic region (MHR) of the hepatitis B virus (HBV) S gene on the expression, secretion, and antigenicity of hepatitis B surface antigen (HBsAg), and evaluate the performance of commonly used commercial HBsAg detection systems in identifying these variants. Methods: Seventeen high-frequency point mutations within the major hydrophilic region (MHR) of the HBV S gene were previously identified in individuals with occult HBV infection. These mutations were introduced into wild-type HBV sequences using site-directed mutagenesis to construct recombinant eukaryotic expression plasmids. Following sequence confirmation, the plasmids were transfected into Huh-7 cells. At 72 hours post-transfection, both culture supernatants and cell lysates were harvested. HBsAg levels were quantified using five commercial detection systems: Roche, Abbott, Autobio, CHIVD, and KHB. Results: Compared with the wild-type strain, T126A (B) and M133I (B) variants presented significantly increased HBsAg levels (P<0.05). Conversely, HBsAg expression was significantly reduced in K122E (B), C124R (B/C), M133T (B), C138R (B), T143S (B), D144G (B), and L162R (C) variants relative to the wild-type (P<0.05). The L162R (C) variant produced no detectable HBsAg in either lysates or supernatants. The C124R (B/C) variant showed higher reactivity on the Abbott and KHB systems, whereas other systems failed to detect it effectively. In contrast, the C138R (B) and M133T (B) variants were detectable in lysates but undetectable in supernatants, suggesting impaired secretion. Among the evaluated systems, Abbott and KHB systems demonstrated comparatively higher sensitivity for variant detection. Conclusion: Of the 17 MHR variants examined, only T126A (B) and M133I (B) enhanced HBsAg detectability. The remaining mutations impaired detection due to decreased expression, secretion defects, or altered antigenicity. Specifically, L162R (C) likely disrupts expression or antigenicity, C138R (B) and M133T (B) impair secretion, and C124R (B/C) alters antigenicity. Most other variants exhibited reduced detectability across systems. Continued refinement of immunoassays is needed to enhance the identification of HBsAg variants in clinical settings.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.