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A novel occludin-targeting monoclonal antibody prevents hepatitis C virus infection in vitro.
Okai, Ken; Ichikawa-Tomikawa, Naoki; Saito, Akira C; Watabe, Tetsuya; Sugimoto, Kotaro; Fujita, Daiki; Ono, Chikako; Fukuhara, Takasuke; Matsuura, Yoshiharu; Ohira, Hiromasa; Chiba, Hideki.
Afiliación
  • Okai K; Department of Basic Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan.
  • Ichikawa-Tomikawa N; Department of Gastroenterology, Fukushima Medical University School of Medicine, Fukushima, Japan.
  • Saito AC; Department of Basic Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan.
  • Watabe T; Department of Basic Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan.
  • Sugimoto K; Department of Basic Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan.
  • Fujita D; Department of Basic Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan.
  • Ono C; Department of Basic Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan.
  • Fukuhara T; Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
  • Matsuura Y; Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
  • Ohira H; Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
  • Chiba H; Department of Gastroenterology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Oncotarget ; 9(24): 16588-16598, 2018 Mar 30.
Article en En | MEDLINE | ID: mdl-29682171
Since hepatitis C virus (HCV) is thought to enter into host hepatocytes using the same cellular pathways regardless of the genotypes, the host factors are promising targets to prevent and treat HCV infection. Human occludin (hOCLN) is one representative entry factor, and its second extracellular loop (EC2) contributes to the species selectivity of HCV-susceptibility. However, the exact function of hOCLN during HCV entry remains unknown, and no hOCLN-targeting antibodies or synthetic drugs that prevent and treat HCV infection have yet been developed. Here we generated the anti-hOCLN-EC2 monoclonal antibody (mAb) 67-2, and demonstrated that it efficiently inhibited HCV infection in the HCV-permissive human cell line Huh7.5.1. We also showed, using three different culture systems of Huh7.5.1 cells, that this novel mAb is accessible to OCLN from the basolateral side of hepatocytes but not from the apical side. In addition, our Western blot analyses indicated that the established 67-2 mAb reacted not only with hOCLN but also with mouse OCLN, strongly suggesting that 67-2 does not recognize the human-specific amino acids in OCLN-EC2. Moreover, we revealed that the anti-hOCLN-EC2 mAb 67-2 showed no adverse effects on cell viability or the barrier function of tight junctions.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Oncotarget Año: 2018 Tipo del documento: Article País de afiliación: Japón

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Oncotarget Año: 2018 Tipo del documento: Article País de afiliación: Japón