北海道大学 · Medicine
타카스케 후쿠하라 교수의 연구실은 간염 C 바이러스(HCV)의 세포 침입 메커니즘과 조직 침범 원리에 중점을 두고 있으며, 특히 miR-122와 아폴리포프로틴(ApoB, ApoE)이 바이러스의 생존과 전파에 미치는 영향을 중심으로 연구를 진행하고 있습니다. 비특이적 세포에서도 HCV의 복제가 가능하게 하는 분자 기전과, 간세포 외부 조직으로의 확산 메커니즘을 규명하고자 합니다. 이는 HCV의 만성 간질환 및 간세포암과 같은 비간질환 합병증의 기전 규명에 기여합니다.
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Hepatitis C virus (HCV) is one of the most common etiologic agents of chronic liver diseases, including liver cirrhosis and hepatocellular carcinoma. In addition, HCV infection is often associated with extrahepatic manifestations (EHM), including mixed cryoglobulinemia and non-Hodgkin's lymphoma. However, the mechanisms of cell tropism of HCV and HCV-induced EHM remain elusive, because in vitro propagation of HCV has been limited in the combination of cell culture-adapted HCV (HCVcc) and several
Apolipoprotein B (ApoB) and ApoE have been shown to participate in the particle formation and the tissue tropism of hepatitis C virus (HCV), but their precise roles remain uncertain. Here we show that amphipathic α-helices in the apolipoproteins participate in the HCV particle formation by using zinc finger nucleases-mediated apolipoprotein B (ApoB) and/or ApoE gene knockout Huh7 cells. Although Huh7 cells deficient in either ApoB or ApoE gene exhibited slight reduction of particles formation, k
Hepatitis C virus (HCV) exhibits a narrow host range and a specific tissue tropism. Mice expressing major entry receptors for HCV permit viral entry, and therefore the species tropism of HCV infection is considered to be reliant on the expression of the entry receptors. However, HCV receptor candidates are expressed and replication of HCV-RNA can be detected in several nonhepatic cell lines, suggesting that nonhepatic cells are also susceptible to HCV infection. Recently it was shown that the ex
