ArticleThe Journal of biological chemistry2010
Hepatitis B virus protein X-induced expression of the CXC chemokine IP-10 is mediated through activation of NF-kappaB and increases migration of leukocytes.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 60 citations in OpenAlex.
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Hepatitis B virus integration and hepatocarcinogenesis.Liver research (Beijing, China) · 2025Review
- IP-10 acts early in CV-A16 infection to induce BBB destruction and promote virus entry into the CNS by increasing TNF-α expression.Frontiers in immunology · 2024Article
- The Role of Plasminogen Activator Inhibitor 1 in Predicting Sepsis-Associated Liver Dysfunction: An Observational Study.International journal of environmental research and public health · 2023Observational
- Review
- Review
- Molecular clones of genetically distinct hepatitis B virus genotypes reveal distinct host and drug treatment responses.JHEP reports : innovation in hepatology · 2022Article
- Regulation of Pattern-Recognition Receptor Signaling by HBX During Hepatitis B Virus Infection.Frontiers in immunology · 2022Review
- Regulation and functional roles of chemokines in liver diseases.Nature reviews. Gastroenterology & hepatology · 2021Review
- Cytokines and Chemokines in HBV Infection.Frontiers in molecular biosciences · 2021Review
- Article
- Distinctiveness in virological features and pathogenic potentials of subgenotypes D1, D2, D3 and D5 of Hepatitis B virus.Scientific reports · 2018Article
- Porcine reproductive and respiratory syndrome virus (PRRSV) up-regulates IL-8 expression through TAK-1/JNK/AP-1 pathways.Virology · 2017Article
- Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis.Oncotarget · 2017Review
- Deregulated MicroRNA-21 Expression in Monocytes from HIV-Infected Patients Contributes to Elevated IP-10 Secretion in HIV Infection.Frontiers in immunology · 2017Article
- Impact of non-neoplastic vs intratumoural hepatitis B viral DNA and replication on hepatocellular carcinoma recurrence.British journal of cancer · 2016Article
- Human hepatocytes express absent in melanoma 2 and respond to hepatitis B virus with interleukin-18 expression.Virus genes · 2016Article
- MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ.RNA (New York, N.Y.) · 2015Article
- Accurately mapping the location of the binding site for the interaction between hepatitis B virus X protein and cytochrome c oxidase III.International journal of molecular medicine · 2015Article
- How did hepatitis B virus effect the host genome in the last decade?World journal of hepatology · 2014Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon-gamma inducible protein 10 (IP-10) involves inflammatory cell recruitment and cellular immune damage during virus infection. Although an increase of the peripheral IP-10 level is known in HBV-infected patients, the molecular basis of HBV infection inducing IP-10 expression has remained elusive. In the present study, we demonstrate that hepatitis B virus protein X (HBx) increases IP-10 expression in a dose-dependent manner. Transfection of the HBx-expressing vector into HepG2 cells results in nuclear translocation of NF-kappaB, which directly binds the promoter of IP-10 at positions from -122 to -113, thus facilitating transcription. The addition of the NF-kappaB inhibitor blocks the effect of HBx on IP-10 induction. In parallel, increase of NF-kappaB subunits p65 and p50 in HepG2 cells also augments IP-10 expression. Furthermore, we show that HBx induces activation of NF-kappaB through the TRAF2/TAK1 signaling pathway, leading to up-regulation of IP-10 expression. As a consequence, up-regulation of IP-10 may mediate the migration of peripheral blood leukocytes in a NF-kappaB-dependent manner. In conclusion, we report a novel molecular mechanism of HBV infection inducing IP-10 expression, which involves viral protein HBx affecting NF-kappaB pathway, leading to transactivation of the IP-10 promoter. Our study provides insight into the migration of leukocytes in response to HBV infection, thus causing immune pathological injury of liver.
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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.