Detail Systematic identification of anti-interferon function on hepatitis C virus genome reveals p7 as an immune evasion protein (from PNAS 2017, 114 (8), 2018-2023) Bibliografi Author: Qi, Hangfei ; Chu, Virginia ; Wu, Nicholas C. ; Chen, Zugen ; Truong, Shawna ; Brar, Gurpreet ; Su, Sheng-Yao ; Du, Yushen ; Arumugaswami, Vaithilingaraja ; Olson, C. Anders ; Chen, Shu-Hua ; Lin, Chung-Yen ; Wu, Ting-Ting ; Sun, Ren Topik: HCV; Innate immune evasion mechanism; IF6-16 antiviral function; High-throughput mutagenesis; P7 ion channel protein; Seminar - Thesis lit Bahasa: (EN )     Tahun Terbit: 2017     Jenis: Article - diterbitkan di jurnal ilmiah internasional Fulltext: PNAS-2017-Qi-2018-23.pdf (1.0MB; 0 download) [Informasi yang berkaitan dengan koleksi ini di internet] Abstract Hepatitis C virus (HCV) encodes mechanisms to evade the multilayered antiviral actions of the host immune system. Great progress has been made in elucidating the strategies HCV employs to downregulate interferon (IFN) production, impede IFN signaling transduction, and impair IFN-stimulated gene (ISG) expression. However, there is a limited understanding of the mechanisms governing how viral proteins counteract the antiviral functions of downstream IFN effectors due to the lack of an efficient approach to identify such interactions systematically. To study the mechanisms by which HCV antagonizes the IFN responses, we have developed a high-throughput profiling platform that enables mapping of HCV sequences critical for anti-IFN function at high resolution. Genome-wide profiling performed with a 15-nt insertion mutant library of HCV showed that mutations in the p7 region conferred high levels of IFN sensitivity,which could be alleviated by the expression ofWT p7 protein. This finding suggests that p7 protein of HCV has an immune evasion function. By screening a liver-specific ISG library, we identified that IFI6-16 significantly inhibits the replication of p7 mutant viruses without affectingWT virus replication. In contrast, knockout of IFI6-16 reversed the IFN hypersensitivity of p7 mutant virus. In addition, p7 was found to be coimmunoprecipitated with IFI6-16 and to counteract the function of IFI6-16 by depolarizing the mitochondria potential. Our data suggest that p7 is a critical immune evasion protein that suppresses the antiviral IFN function by counteracting the function of IFI6-16. [seminar - thesis lit] Opini Anda Klik untuk menuliskan opini Anda tentang koleksi ini! Lihat Sejarah Pengadaan  Konversi Metadata   Kembali

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