ArticlePloS one2025
Identification of novel antiviral host factors by functional gene expression analysis using in vitro HBV infection assay systems.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Article
- Dermatopathic Lymphadenopathy withInfection and drug resistance · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To cure hepatitis B virus (HBV) infection, it is essential to elucidate the function of hepatocyte host factors in regulating the viral life cycle. Signaling and transcription activator of transcription (STAT)1 play important roles in immune responses, but STAT1-independent pathways have also been shown to have important biological reactivity. Using an in vitro HBV infection assay system, the current study aimed to investigate the STAT1-independent host factors that contribute to the control of viral infection by comprehensive functional screening. The in vitro HBV infection system was established using primary human hepatocytes (PXB cells) infected with HBV derived from a plasmid containing the 1.3-mer HBV genome. Comprehensive functional studies were performed using small interfering RNA (siRNA) and vector transfection and analyzed using microarrays. Knockdown of STAT1 increased viral products in HBV-transfected HepG2 cells, but decreased in HBV-infected PXB cells. RNA microarray was performed using HBV-infected PXB cells with STAT1 knockdown. Fumarylacetoacetate hydrolase (FAH) was extracted by siRNA of genes in PXB cells altered by STAT1 knockdown. Transfection of FAH inhibited HBV replication. Dimethyl fumarate (DMF), the methyl ester of FAH metabolite, showed antiviral effects by inducing autophagy and anti-HBV-related genes. Independently of STAT1, FAH was identified as a host factor that contributes to the control of viral infection, and its metabolite, DMF, exhibited antiviral activity. These results suggest that the novel host factor FAH and its metabolites may be an innovative therapeutic strategy to control the HBV life cycle.
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.