ArticleThe Journal of infectious diseases2014
Natural cytotoxicity receptor-dependent natural killer cytolytic activity directed at hepatitis C Virus (HCV) is associated with liver inflammation, African American race, IL28B genotype, and response to pegylated interferon/ribavirin therapy in chronic HCV infection.
Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Innate Immune Activity Correlates with CD4 T Cell-Associated HIV-1 DNA Decline during Latency-Reversing Treatment with Panobinostat.Journal of virology · 2015Trial
- CD56Journal of leukocyte biology · 2017Article
- Concerted action of IFN-α and IFN-λ induces local NK cell immunity and halts cancer growth.Oncotarget · 2016Article
- Spontaneous and natural cytotoxicity receptor-mediated cytotoxicity are effector functions of distinct natural killer subsets in hepatitis C virus-infected chimpanzees.Clinical and experimental immunology · 2016Article
- HBD-3 induces NK cell activation, IFN-γ secretion and mDC dependent cytolytic function.Cellular immunology · 2015Article
- Regulation of Interferon-Stimulated Gene BST2 by a lncRNA Transcribed from a Shared Bidirectional Promoter.Frontiers in immunology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNatural killer (NK) cells are implicated in the pathogenesis of hepatitis C virus (HCV) infection and outcome of interferon (IFN)-α based therapy, although mechanisms remain unclear.
methodsTo evaluate NK ability to control HCV infection, we analyzed healthy donor and HCV-infected donor NK-cell cytolytic activity directed at HCV-infected target cells.
resultsHCV-infected subjects' natural cytotoxicity receptor (NCR)-dependent NK-cell cytolytic activity directed at HCV-infected and uninfected Huh7.5 target cells was greater than that of cells from healthy donors, and this localized to the African American subset. However, IFN-α-enhanced NK cytolytic function was lower in HCV-infected subjects, again localized mainly to the African American subset. Additionally, whereas HCV-infected Huh7.5 cells were more readily targeted than uninfected cells, the selectivity of cytolytic activity for infected targets was lower during HCV infection and after IFN-α stimulation, and lower selectivity was in part attributable to greater NKp46 expression. Furthermore, cytolytic activity was associated with higher serum aspartate aminotransferase, rs12979860 IL28B genotype, and in vivo response to pegylated IFN/ribavirin therapy.
conclusionsThese data indicate that during chronic HCV infection, race-associated increase in NCR expression and IL28B-associated cytolytic activity may participate in host response to IFN-α-containing HCV therapy.
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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 OpenQuestion graph.