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The J6JFH1 Strain of Hepatitis C Virus Infects Human B-Cells with Low Replication Efficacy

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Title: The J6JFH1 Strain of Hepatitis C Virus Infects Human B-Cells with Low Replication Efficacy
Authors: Nakai, Masato Browse this author
Seya, Tsukasa Browse this author →KAKEN DB
Matsumoto, Misako Browse this author →KAKEN DB
Shimotohno, Kunitada Browse this author
Sakamoto, Naoya Browse this author →KAKEN DB
Aly, Hussein H. Browse this author
Issue Date: Aug-2014
Publisher: Mary Ann Liebert
Journal Title: Viral Immunology
Volume: 27
Issue: 6
Start Page: 285
End Page: 294
Publisher DOI: 10.1089/vim.2013.0140
PMID: 24853207
Abstract: Hepatitis C virus (HCV) infection is a serious health problem worldwide that can lead to hepatocellular carcinoma or end-stage liver disease. Current treatment with pegylated interferon, ribavirin, and NS3/4A protease inhibitor would lead to a good prognosis in a large population of patients, but there is still no effective vaccine for HCV. HCV robustly infects hepatocytes in the liver. However, extrahepatic manifestations such as mixed cryoglobulinemia, a systemic immune complex-mediated disorder characterized by B-cell proliferation, which may evolve into overt B-cell non-Hodgkin's lymphoma, have been demonstrated. HCV-RNA is often found to be associated with peripheral blood lymphocytes, suggesting a possible interaction with peripheral blood mononuclear cells (PBMCs), especially B-cells with HCV. B-cell HCV infection was a matter of debate for a long time, and the new advance in HCV in vitro infectious systems suggest that exosome can transmit HCV genome to support "infection." We aimed to clarify the susceptibility of primary B-cells to HCV infection, and to study its functional effect. In this article, we found that the recombinant HCV J6JFH1 strain could infect human B-cells isolated from the peripheral blood of normal volunteers by the detection of both HCV-negative-strand RNA by reverse transcription polymerase chain reaction, and NS5A protein. We also show the blocking of HCV replication by type I interferon after B-cell HCV infection. Although HCV replication in B-lymphocytes showed lower efficiency, in comparison with hepatocyte line (Huh7) cells, our results clearly demonstrate that human B-lymphocytes without other non-B-cells can actually be infected with HCV, and that this interaction leads to the induction of B-cells' innate immune response, and change the response of these cells to apoptosis.
Rights: This is a copy of an article published in the Viral Immunology © 2014 copyright Mary Ann Liebert, Inc.; Viral Immunology is available online at:
Type: article
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 瀬谷 司

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