ArticleScientific reports2017
CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Interferon Regulatory Factor 3 as a Mediator and Therapeutic Target in Innate Immune-Driven Corneal Stromal Inflammation and Opacity.Investigative ophthalmology & visual science · 2026Article
- Reconstitution of interferon regulatory factor 7 expression restores interferon beta induction in Huh7 cells.Journal of virology · 2025Article
- Redefining the immune landscape of hepatitis A virus infection.Experimental & molecular medicine · 2025Review
- Limited impact of hepatitis A virus 3C protease-mediated cleavage on the functions of NEMO in human hepatocytes.Journal of virology · 2025Article
- Liver diseases: epidemiology, causes, trends and predictions.Signal transduction and targeted therapy · 2025Review
- Seneca valley virus VP4 protein regulates the transcription of different cytokinesFrontiers in veterinary science · 2025Article
- The Role of Interferon Regulatory Factors in Liver Diseases.International journal of molecular sciences · 2024Review
- Biochemical analysis of the host factor activity of ZCCHC14 in hepatitis A virus replication.Journal of virology · 2024Article
- Effects ofFoods (Basel, Switzerland) · 2023Article
- Hepatitis A: Viral Structure, Classification, Life Cycle, Clinical Symptoms, Diagnosis Error, and Vaccination.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2023Review
- Intrahepatic infiltration of activated CD8Frontiers in immunology · 2023Article
- Review
- Latent Cytomegalovirus-Driven Recruitment of Activated CD4+ T Cells Promotes Virus Reactivation.Frontiers in immunology · 2021Article
- Circulating Cytokines and Coronavirus Disease: A Bi-Directional Mendelian Randomization Study.Frontiers in genetics · 2021Article
- Co-Occurrence of Hepatitis A Infection and Chronic Liver Disease.International journal of molecular sciences · 2020Review
- EpCAM-high liver cancer stem cells resist natural killer cell-mediated cytotoxicity by upregulating CEACAM1.Journal for immunotherapy of cancer · 2020Article
- Rotavirus Reprograms Multiple Interferon Receptors and Restricts Their Intestinal Antiviral and Inflammatory Functions.Journal of virology · 2020Article
- Article
- Unique Roles forFrontiers in immunology · 2020Article
- Innate Immune Response to Influenza Virus at Single-Cell Resolution in Human Epithelial Cells Revealed Paracrine Induction of Interferon Lambda 1.Journal of virology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute hepatitis A caused by hepatitis A virus (HAV) infection is accompanied by severe liver injury in adult patients, and the liver injury is associated with the production of chemokines. Herein, we investigated the mechanism of how HAV infection induces the production of CXCR3 and CCR5 chemokines, such as CXCL10, CCL4 and CCL5. The production of CXCL10, CCL4 and CCL5 was markedly increased by HAV (HM-175/18f) infection in the culture of primary human hepatocytes and HepG2 cells. In particular, CXCL10 was produced in HAV-infected cells, not in neighboring uninfected cells. Moreover, these chemokines were significantly increased in the sera of acute hepatitis A patients. The production of IFN-λs was also robustly induced by HAV infection, and the blocking of secreted IFN-λs partially abrogated the production of CCL4 and CCL5 in HAV-infected cells. However, CXCL10 production was not decreased by the blocking of IFN-λs. Instead, CXCL10 production was reduced by silencing the expression of RIG-I-like receptor (RLR) signal molecules, such as mitochondrial antiviral signaling protein and interferon regulatory factor 3, in HAV-infected cells. In conclusion, HAV infection strongly induces the production of helper 1 T cell-associated chemokines, particularly CXCL10 via RLR signaling, even without secreted IFNs.
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