ArticlePLoS pathogens2017
Hepatitis C virus infection inhibits a Src-kinase regulatory phosphatase and reduces T cell activation in vivo.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Human Pegivirus Infection and Lymphoma Risk: A Systematic Review and Meta-analysis.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2020Pooled it
- Integrated multiomics reveals host-virus coadaptation in persistent foot-and-mouth disease virus infection.Cellular and molecular life sciences : CMLS · 2025Article
- Characterization of Serotype-Specific Dengue Virus T-Cell Inhibition.The Journal of infectious diseases · 2025Article
- Characterization of "Off-Target" Immune Modulation Induced by Live Attenuated Yellow Fever Vaccine.The Journal of infectious diseases · 2024Article
- CMV specific T cell immune response in hepatitis C negative kidney transplant recipients receiving transplant from hepatitis C viremic donors and hepatitis C aviremic donors.Renal failure · 2022Article
- A short hepatitis C virus NS5A peptide expression by AAV vector modulates human T cell activation and reduces vector immunogenicity.Gene therapy · 2022Article
- Association of donor hepatitis C virus infection status and risk of BK polyomavirus viremia after kidney transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
- The LncRNA, the phosphatase, and the macrophage: can they team up for support in inflammatory diseases?Annals of translational medicine · 2020Article
- Modulation of TCR Signaling by Tyrosine Phosphatases: From Autoimmunity to Immunotherapy.Frontiers in cell and developmental biology · 2020Review
- Laboratory Diagnosis and Monitoring of Viral Hepatitis.Gastroenterology clinics of North America · 2019Review
- Human Pegivirus infection and lymphoma risk and prognosis: a North American study.British journal of haematology · 2018Article
- Yellow Fever Virus, but Not Zika Virus or Dengue Virus, Inhibits T-Cell Receptor-Mediated T-Cell Function by an RNA-Based Mechanism.The Journal of infectious diseases · 2017Article
- Dysregulated epidermal growth factor and tumor growth factor-beta receptor signaling throughPakistan journal of medical sciencesArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Among human RNA viruses, hepatitis C virus (HCV) is unusual in that it causes persistent infection in the majority of infected people. To establish persistence, HCV evades host innate and adaptive immune responses by multiple mechanisms. Recent studies identified virus genome-derived small RNAs (vsRNAs) in HCV-infected cells; however, their biological significance during human HCV infection is unknown. One such vsRNA arising from the hepatitis C virus (HCV) E2 coding region impairs T cell receptor (TCR) signaling by reducing expression of a Src-kinase regulatory phosphatase (PTPRE) in vitro. Since TCR signaling is a critical first step in T cell activation, differentiation, and effector function, its inhibition may contribute towards HCV persistence in vivo. The effect of HCV infection on PTPRE expression in vivo has not been examined. Here, we found that PTPRE levels were significantly reduced in liver tissue and peripheral blood mononuclear cells (PBMCs) obtained from HCV-infected humans compared to uninfected controls. Loss of PTPRE expression impaired antigen-specific TCR signaling, and curative HCV therapy restored PTPRE expression in PBMCs; restoring antigen-specific TCR signaling defects. The extent of PTPRE expression correlated with the amount of sequence complementarity between the HCV E2 vsRNA and the PTPRE 3' UTR target sites. Transfection of a hepatocyte cell line with full-length HCV RNA or with synthetic HCV vsRNA duplexes inhibited PTPRE expression, recapitulating the in vivo observation. Together, these data demonstrate that HCV infection reduces PTPRE expression in the liver and PBMCs of infected humans, and suggest that the HCV E2 vsRNA is a novel viral factor that may contribute towards viral persistence.
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