Evidence map›Paper›PMID 41346365›Full record

ReviewFrontiers in cellular and infection microbiology2025

Unveiling low level viremia in chronic hepatitis B: challenges and new horizons.

Bingqing Wang, Tian Zeng, Wen Yin, Chengrui Ren, Yuting Chen, Liqin Qian, Peng Huang, Chuanlong Zhu, Ming Yue

Abstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Bingqing Wang *Department of Infectious Diseases, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.
Tian Zeng *Department of Infectious Diseases, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.
Wen Yin *Department of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Chengrui RenDepartment of Infectious Diseases, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.
Yuting ChenDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Liqin QianDepartment of Infectious Diseases, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.
Peng HuangDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Chuanlong ZhuDepartment of Infectious Diseases, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.
Ming YueDepartment of Infectious Diseases, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low-level viremia (LLV) in chronic hepatitis B (CHB) represents a significant challenge and area of interest in current clinical management. While nucleos (t)ide analogs (NAs) have demonstrated substantial efficacy in suppressing hepatitis B virus (HBV) replication, the application of highly sensitive detection methods has revealed that some treated patients continue to exhibit persistent or intermittent low-level viremia (HBV DNA: 12-2000 IU/mL). The mechanisms underlying LLV involve a synergistic interplay between host immune response deficiencies and HBV covalently closed circular DNA (cccDNA) persistence. Furthermore, the complex regulation of LLV is influenced by metabolic-associated steatotic liver disease (MASLD). Limitations in the clearance of cccDNA by current antiviral regimens also contribute to this phenomenon. LLV may elevate the risk of liver fibrosis progression, hepatocellular carcinoma (HCC), and end-stage liver disease. Current management strategies emphasize optimizing antiviral regimens, such as switching to tenofovir alafenamide (TAF) or combining therapies with pegylated interferon-alpha (Peg-IFN-α). Enhanced dynamic monitoring, including high-sensitivity HBV DNA assays and quantitative hepatitis B surface antigen (HBsAg) measurements, is also crucial. Moreover, exploring combination therapies involving immunomodulation and hepatocyte regeneration is warranted. Further research should integrate multi-omics technologies with prospective cohort studies to elucidate the host-virus interaction network in LLV. This will allow for the validation of synergistic effects between metabolic interventionsand immunotherapy, thereby advancing personalized precision medicine. This review systematically synthesizes the epidemiological characteristics, pathogenesis, influencing factors, prognosis, and clinical management advancements of LLV, aiming to provide novel perspectives for optimizing therapeutic strategies and translational research.

Indexed as

Hepatitis B, ChronicHepatitis B virusViremiaAntiviral AgentsDNA, CircularDNA, ViralHepatitis B Surface AntigensHumansViral LoadVirus ReplicationAntiviral AgentsDNA, CircularDNA, ViralHepatitis B Surface Antigenschronic hepatitis Bclinical remissionfatty liver diseaselow level viremianucleos(t) ide analogspeginterferon

Identifiers

PMID41346365
PMCPMC12672879

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.