ArticleHepatology (Baltimore, Md.)2018
Hepatitis B Virus Evasion From Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase Sensing in Human Hepatocytes.
Article in Hepatology (Baltimore, Md.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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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.
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Who cites it
70 citing papers in PubMed, 94 citations in OpenAlex.
- The Significance of cGAS-STING Signaling in Response to Oncogenic Viruses.Cell biochemistry and function · 2026Review
- The diversity of STING in regulating immune cell function and its role in liver diseases: from bench to bedside.Cell & bioscience · 2026Review
- Regulation of immune tolerance in hepatocellular carcinoma by liver diseases: a review.Infectious agents and cancer · 2026Review
- Functional immune responses induced by a capsid assembly modulator in chronic hepatitis B virus-infected humanized mice.Cell host & microbe · 2026Article
- Innate immune recognition and evasion strategies of hepatitis B virus: from DNA to RNA and viral proteins.Frontiers in immunology · 2026Review
- Innate immune recognition in hepatitis B virus infection.Virulence · 2025Review
- New mechanistic understanding of FXR agonist Vonafexor: inducing sublethal damage of HBV-positive liver cancer cells via promoting anti-tumor immunity.British journal of cancer · 2025Article
- Hepatocyte-intrinsic innate immunity in hepatitis B virus infection: A focused review.World journal of hepatology · 2025Review
- Adeno-associated virus 2 CRISPR/Cas9-mediated targeting of hepatitis B virus in tree shrews.Virus research · 2025Article
- Universal STING Pathway-Activating Complexes Counteract Viral Immune Evasion and Boost Antiviral Responses.ACS nano · 2025Article
- Hepatitis B virus confers innate immunity evasion through hepatitis B virus-miR-3 down-regulation of cGAS-Sting-IFN signaling.World journal of hepatology · 2025Article
- The role of cGAS-STING signaling in the liver and gastrointestinal system: from signaling networks to target intervention.Frontiers in immunology · 2025Review
- Targeting cGAS-STING: modulating the immune landscape of hepatic diseases.Frontiers in immunology · 2025Review
- cGAS-STING pathway as a promising target for digestive diseases: insights from natural plant products.Frontiers in nutrition · 2025Review
- [Immune status of inactive HBsAg antigen carriers with chronic HBV infection].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024Article
- Mechanisms underlying the compromised clinical efficacy of interferon in clearing HBV.Virology journal · 2024Review
- CAM-A-dependent HBV core aggregation induces apoptosis through ANXA1.JHEP reports : innovation in hepatology · 2024Article
- The dual function of cGAS-STING signaling axis in liver diseases.Acta pharmacologica Sinica · 2024Review
- cGAS suppresses hepatocellular carcinoma independent of its cGAMP synthase activity.Cell death and differentiation · 2024Article
- Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 3 countries.
Funding
Abstract
Chronic hepatitis B virus (HBV) infection is a major cause of chronic liver disease and cancer worldwide. The mechanisms of viral genome sensing and the evasion of innate immune responses by HBV infection are still poorly understood. Recently, the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) was identified as a DNA sensor. In this study, we investigated the functional role of cGAS in sensing HBV infection and elucidate the mechanisms of viral evasion. We performed functional studies including loss-of-function and gain-of-function experiments combined with cGAS effector gene expression profiling in an infectious cell culture model, primary human hepatocytes, and HBV-infected human liver chimeric mice. Here, we show that cGAS is expressed in the human liver, primary human hepatocytes, and human liver chimeric mice. While naked relaxed-circular HBV DNA is sensed in a cGAS-dependent manner in hepatoma cell lines and primary human hepatocytes, host cell recognition of viral nucleic acids is abolished during HBV infection, suggesting escape from sensing, likely during packaging of the genome into the viral capsid. While the hepatocyte cGAS pathway is functionally active, as shown by reduction of viral covalently closed circular DNA levels in gain-of-function studies, HBV infection suppressed cGAS expression and function in cell culture models and humanized mice. Conclusion: HBV exploits multiple strategies to evade sensing and antiviral activity of cGAS and its effector pathways.
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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.