دورية أكاديمية
أعرض في EDS

Recent advances in the anti-HCV mechanisms of interferon.

التفاصيل البيبلوغرافية
العنوان: Recent advances in the anti-HCV mechanisms of interferon.
المؤلفون: Huang M; Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China., Jiang JD; Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China ; Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China., Peng Z; Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
المصدر: Acta pharmaceutica Sinica. B [Acta Pharm Sin B] 2014 Aug; Vol. 4 (4), pp. 241-7. Date of Electronic Publication: 2014 Jul 14.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 101600560 Publication Model: Print-Electronic Cited Medium: Print ISSN: 2211-3835 (Print) Linking ISSN: 22113835 NLM ISO Abbreviation: Acta Pharm Sin B Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Amsterdam] : Elsevier, 2011-
مستخلص: Interferon (IFN) in combination with ribavirin has been the standard of care (SOC) for chronic hepatitis C for the past few decades. Although the current SOC lacks the desired efficacy, and 4 new direct-acting antiviral agents have been recently approved, interferons are still likely to remain the cornerstone of therapy for some time. Moreover, as an important cytokine system of innate immunity, host interferon signaling provides a powerful antiviral response. Nevertheless, the mechanisms by which HCV infection controls interferon production, and how interferons, in turn, trigger anti-HCV activities as well as control the outcome of HCV infection remain to be clarified. In this report, we review current progress in understanding the mechanisms of IFN against HCV, and also summarize the knowledge of induction of interferon signaling by HCV infection.
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فهرسة مساهمة: Keywords: Antiviral agent; CHC, chronic hepatitis C; DCs, dendritic cells; DNAM1, DNAX accessory molecule-1; E2, envelop 2; GAS, IFN-γ-activated site; GWAS, genome-wide association studies; Hepatitis C virus; IFN, interferon; IFN-α, interferon-α; IFNAR1, interferon-alpha receptor 1; IFNAR2, interferon-alpha receptor 2; IFNGR1, interferon gamma receptor 1; IFNGR2, interferon gamma receptor 2; IFNL4, IFN-lambda 4; IL-10R2, interleukin-10 receptor 2; IL-29, interleukin-29; IRF-3, interferon regulatory factor 3; IRGs, IFN regulatory genes; ISG15, interferon-stimulated gene 15; ISGF3, IFN-stimulated gene factor 3; ISGs, IFN-stimulated genes; ISREs, IFN-stimulated response elements; Interferon; JAKs, Janus activated kinases; MAVS, mitochondrial antiviral signaling protein; MDA-5, melanoma differentiation-associated gene-5; MHC, major histocompatibility complex; Molecular mechanism; NKCs, natural killer cells; NKTCs, natural killer T cells; OAS, 2′-5′-oligoadenylate synthetase; PAMPs, pathogen-associated molecular patterns; PBMCs, peripheral blood mononuclear cells; PKR, protein kinase R; PRRs, pattern recognition receptors; RIG-I, retinoic acid-inducible gene-I; RLRs, RIG-I-like receptors; RdRp, RNA dependent RNA polymerase; SNPs, single-nucleotide polymorphisms; SOC, standard of care; STAT1, signal transducer and activator of transcription 1; STAT2, signal transducer and activator of transcription 2; SVR, sustained virological response; TH1, T-helper-1; TH2, T-helper-2; TLRs, Toll-like receptors; TYK2, tyrosine kinase 2; USP18, ubiquitin specific peptidase 18; dsRNA, double-stranded RNA; pDC, plasmacytoid dendritic cell
تواريخ الأحداث: Date Created: 20151119 Date Completed: 20151120 Latest Revision: 20200930
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC4629091
DOI: 10.1016/j.apsb.2014.06.010
PMID: 26579391
قاعدة البيانات: MEDLINE
الوصف
تدمد:2211-3835
DOI:10.1016/j.apsb.2014.06.010