Hokkaido University · 의학
Naoya Sakamoto 교수의 연구실은 간염 바이러스, 특히 간염 C 바이러스(HCV)의 숙주 면역 회피 메커니즘과 바이러스 복제 조절을 중심으로 한 항바이러스 연구를 수행하고 있습니다. 특히 NS5B 및 NS4B 단백질이 숙주 인터페론 신호 경로를 어떻게 억제하는지, 그리고 핵산 기반 치료 전략(예: 해머헤드 리보자임)의 항바이러스 효과를 규명하는 데 초점을 맞추고 있습니다. 이는 바이러스의 만성 감염 유지를 이해하고 새로운 치료 전략 개발에 기여하고자 하는 학문적 목표를 담고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Binding of the HCV-NS5B protein to GBP-1 countered the antiviral effect by inhibition of its GTPase activity. These mechanisms may contribute to resistance to innate, IFN-mediated antiviral defense and to the clinical persistence of HCV infection.
NS4B suppresses RIG-I-mediated IFN-β production signaling through a direct protein interaction with STING. Disruption of that interaction may restore cellular antiviral responses and may constitute a novel therapeutic strategy for the eradication of HCV.
To determine the effects of hammerhead ribozymes against hepatitis C virus (HCV) RNA on viral protein translation, a luciferase reporter gene vector, pCMV/T7-NCRCdelta-luc, was constructed containing the 5'-noncoding region (5'-NCR) and part of the core region of HCV. Four ribozymes, Rz1-Rz4, were designed to cleave at nucleotide positions 136-160, 313-337, 496-520, and 373-388, respectively. Each ribozyme cleaved the target RNA at expected positions under cell-free conditions. Rz2 and Rz4 signi
Cellular antiviral responses are mediated partly by the expression of interferon-stimulated genes, triggered by viral genomes, their transcripts and replicative intermediates. Persistent replication of a hepatitis C virus (HCV) replicon suggests that the replicon does not elicit cellular innate antiviral responses. In the present study, we investigated regulatory factors of the interferon-mediated antiviral system in cells expressing an HCV replicon. Luciferase reporter assays revealed that the
