ArticleFrontiers in microbiology2019
NF-κB-Dependent IFIT3 Induction by HBx Promotes Hepatitis B Virus Replication.
Article in Frontiers in microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- The IFIT3 Protein of Porcine Induces Interferon Signaling and Inhibits the Early Gene Expression of African Swine Fever Virus.Viruses · 2026Article
- NSP1 of Alongshan virus antagonizes type I interferon responses by promoting STUB1-mediated degradation of RIG-I.Cell communication and signaling : CCS · 2026Article
- Article
- Interferon-induced miR-7705 modulates the anti-virus activity of cholesterol 25-hydroxylase.Journal of virology · 2025Article
- HBc: the multifunctional architect of HBV replication, immune evasion, and therapeutic innovation.Frontiers in immunology · 2025Review
- RNF5 inhibits HBV replication by mediating caspase-3-dependent degradation of core protein.Frontiers in microbiology · 2025Article
- ETV7 promotes colorectal cancer progression through upregulation of IFIT3.Functional & integrative genomics · 2024Article
- Cholesterol metabolism regulator SREBP2 inhibits HBV replication via suppression of HBx nuclear translocation.Frontiers in immunology · 2024Article
- Baicalin inhibits the replication of the hepatitis B virus by targeting TRIM25.Journal of traditional and complementary medicine · 2023Article
- Type I/type III IFN and related factors regulate JEV infection and BBB endothelial integrity.Journal of neuroinflammation · 2023Article
- Editorial: Interferon and its antiviral effect in response to HBV infection.Frontiers in immunology · 2023Article
- Decoding the spatial chromatin organization and dynamic epigenetic landscapes of macrophage cells during differentiation and immune activation.Nature communications · 2022Article
- Exploration of immune infiltration and feature genes in viral hepatitis-associated liver fibrosis using transcriptome data.Annals of translational medicine · 2022Article
- LncRNA RP5-998N21.4 promotes immune defense through upregulation of IFIT2 and IFIT3 in schizophrenia.Schizophrenia (Heidelberg, Germany) · 2022Article
- Regulation of Pattern-Recognition Receptor Signaling by HBX During Hepatitis B Virus Infection.Frontiers in immunology · 2022Review
- Downregulation of interferon-induced protein with tetratricopeptide repeats 3 relieves the inflammatory response and myocardial fibrosis of mice with myocardial infarction and improves their cardiac function.Experimental animals · 2021Article
- Identification of significant alteration genes, pathways and TFs induced by LPS in ARDS via bioinformatical analysis.BMC infectious diseases · 2021Article
- Blood Transcriptomes of Anti-SARS-CoV-2 Antibody-Positive Healthy Individuals Who Experienced AsymptomaticFrontiers in immunology · 2021Article
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 at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Therapeutic administration of type I IFN (IFN-I) is a common treatment option for individuals suffering from hepatitis B virus (HBV) infection. IFN-I therapy, however, has a relatively low response rate in HBV-infected patients and can induce serious side-effects, limiting its clinical efficacy. There is, thus, a clear need to understand the molecular mechanisms governing the influence of IFN-I therapy in HBV treatment in order to improve patient outcomes. In this study, we explored the interactions between HBV and IFITs (IFN-induced proteins with tetratricopeptide repeats), which are classical IFN-inducible genes. Specifically, we found that HBV patients undergoing IFN-I therapy exhibited elevated expression of IFITs in their peripheral blood mononuclear cells (PBMCs). We further observed upregulation in the expressions of IFIT1, IFIT2, and IFIT3 in cells transfected with the pHBV1.3 plasmid, which yields infectious virions in hepatic cells. We additionally found that HBx, which is the only regulatory protein encoded within the HBV genome, activates NF-κB, which in turn directly drives IFIT3 transcription. When IFIT3 was overexpressed in HepG2 cells, HBV replication was enhanced. Together, these results suggest that IFIT genes may unexpectedly enhance viral replication, thus making these genes potential therapeutic targets in patients with HBV.
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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.