Impact of hepatitis C virus infection in B cells on pathogenesis

点击翻译按钮获取中文摘要

Hepatitis C virus (HCV) infection leads to the development of hepatic diseases, as well as extra hepatic disorders such as B-cell non-Hodikin's lymphoma (B-NHL). To reveal the molecular signaling pathways responsible for HCV-associated B-NHL development, we utilized transgenic (Tg) mice that express the full-length HCV genome specifically in B cells and develop non-Hodgkin type B-cell lymphomas (BCLs). The gene expression profiles in B cells from BCL-developing HCV-Tg mice, from BCL-non-deceloping HCV-Tg mice, and from BCL-non-developing HCV-negative mice were analyzed by genome-wide microarray.Markedly modified genes such as Fos, C3, LTbR, A20, NF-kB and miR-26b in BCLs were further characterized using specific assays. We propose that activation of both canonical and alternative NF-kB signaling pathways and down-regulation of miR-26b contribute to the development of HCV-associated B-NHL.