ArticleNature communications2020
A genome-wide gain-of-function screen identifies CDKN2C as a HBV host factor.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Key hub genes and pathways associated with HCV-related hepatocellular carcinoma as potential diagnostic biomarkers.Journal, genetic engineering & biotechnology · 2026Article
- Orthogonal CRISPR screens and human liver chimeric mice identify hepatitis B virus host factors.bioRxiv : the preprint server for biology · 2026Article
- Hepatitis B core-related antigen as a promising serological marker for monitoring hepatitis B virus cure.World journal of hepatology · 2025Review
- Article
- CAM-A-dependent HBV core aggregation induces apoptosis through ANXA1.JHEP reports : innovation in hepatology · 2024Article
- Screening and molecular docking verification of feature genes related to phospholipid metabolism in hepatocarcinoma caused by hepatitis B.Lipids in health and disease · 2024Article
- Article
- Article
- Long-Term Hepatitis B Virus Infection Induces Cytopathic Effects in Primary Human Hepatocytes, and Can Be Partially Reversed by Antiviral Therapy.Microbiology spectrum · 2022Article
- The cytoplasmic LSm1-7 and nuclear LSm2-8 complexes exert opposite effects on Hepatitis B virus biosynthesis and interferon responses.Frontiers in immunology · 2022Article
- Hepatitis B virus-host interactions and novel targets for viral cure.Current opinion in virology · 2021Review
- Elevated NTCP expression by an iPSC-derived human hepatocyte maintenance medium enhances HBV infection in NTCP-reconstituted HepG2 cells.Cell & bioscience · 2021Article
- Downregulation of HBx Restrains Proliferation, Migration, and Invasion of HepG2 Cells.Analytical cellular pathology (Amsterdam) · 2021Article
- Article
Corrections and comments
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Authors and funding
23 authors at 7 institutions in 5 countries.
Funding
Abstract
Chronic HBV infection is a major cause of liver disease and cancer worldwide. Approaches for cure are lacking, and the knowledge of virus-host interactions is still limited. Here, we perform a genome-wide gain-of-function screen using a poorly permissive hepatoma cell line to uncover host factors enhancing HBV infection. Validation studies in primary human hepatocytes identified CDKN2C as an important host factor for HBV replication. CDKN2C is overexpressed in highly permissive cells and HBV-infected patients. Mechanistic studies show a role for CDKN2C in inducing cell cycle G1 arrest through inhibition of CDK4/6 associated with the upregulation of HBV transcription enhancers. A correlation between CDKN2C expression and disease progression in HBV-infected patients suggests a role in HBV-induced liver disease. Taken together, we identify a previously undiscovered clinically relevant HBV host factor, allowing the development of improved infectious model systems for drug discovery and the study of the HBV life cycle.
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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 Socratic graph.