2024-03-28T13:29:23Zhttps://eprints.lib.hokudai.ac.jp/dspace-oai/requestoai:eprints.lib.hokudai.ac.jp:2115/568712022-11-17T02:08:08Zhdl_2115_20040hdl_2115_121The J6JFH1 Strain of Hepatitis C Virus Infects Human B-Cells with Low Replication EfficacyNakai, MasatoSeya, TsukasaMatsumoto, MisakoShimotohno, KunitadaSakamoto, NaoyaAly, Hussein H.490Hepatitis 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.Mary Ann LiebertJournal Articleapplication/pdfhttp://hdl.handle.net/2115/56871https://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/56871/1/Viral%20Immunol_27%286%29_285-294.pdf0882-8245Viral Immunology2762852942014-08enginfo:pmid/24853207info:doi/10.1089/vim.2013.0140This is a copy of an article published in the Viral Immunology © 2014 copyright Mary Ann Liebert, Inc.; Viral Immunology is available online at: http://online.liebertpub.com.publisher