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@ARTICLE{Alberione:886069,
      author       = {Alberione, María Pía and Moeller, Rebecca and Kirui,
                      Jared and Ginkel, Corinne and Doepke, Mandy and Ströh,
                      Luisa J. and Machtens, Jan-Philipp and Pietschmann, Thomas
                      and Gerold, Gisa},
      title        = {{S}ingle-nucleotide variants in human {CD}81 influence
                      hepatitis {C} virus infection of hepatoma cells},
      journal      = {Medical microbiology and immunology},
      volume       = {209},
      number       = {4},
      issn         = {1432-1831},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {FZJ-2020-04255},
      pages        = {499 - 514},
      year         = {2020},
      abstract     = {An estimated number of 71 million people are living with
                      chronic hepatitis C virus (HCV) infection worldwide and
                      400,000 annual deaths are related to the infection. HCV
                      entry into the hepatocytes is complex and involves several
                      host factors. The tetraspanin human CD81 (hCD81) is one of
                      the four essential entry factors and is composed of one
                      large extracellular loop, one small extracellular loop, four
                      transmembrane domains, one intracellular loop and two
                      intracellular tails. The large extracellular loop interacts
                      with the E2 glycoprotein of HCV. Regions outside the large
                      extracellular loop (backbone) of hCD81 have a critical role
                      in post-binding entry steps and determine susceptibility of
                      hepatocytes to HCV. Here, we investigated the effect of five
                      non-synonymous single-nucleotide variants in the backbone of
                      hCD81 on HCV susceptibility. We generated cell lines that
                      stably express the hCD81 variants and infected the cells
                      using HCV pseudoparticles and cell culture-derived HCV. Our
                      results show that all the tested hCD81 variants support HCV
                      pseudoparticle entry with similar efficiency as wild-type
                      hCD81. In contrast, variants A54V, V211M and M220I are less
                      supportive to cell culture-derived HCV infection. This
                      altered susceptibility is HCV genotype dependent and
                      specifically affected the cell entry step. Our findings
                      identify three hCD81 genetic variants that are impaired in
                      their function as HCV host factors for specific viral
                      genotypes. This study provides additional evidence that
                      genetic host variation contributes to inter-individual
                      differences in HCV infection and outcome.},
      cin          = {IBI-1 / JARA-HPC},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IBI-1-20200312 / $I:(DE-82)080012_20140620$},
      pnm          = {551 - Functional Macromolecules and Complexes (POF3-551) /
                      MOLECULAR MODELLING OF BIFUNCTIONAL MEMBRANE TRANSPORT
                      PROTEINS $(jics40_20190501)$ / Multiscale simulations of
                      voltage-gated sodium channel complexes and clusters
                      $(jics42_20191101)$},
      pid          = {G:(DE-HGF)POF3-551 / $G:(DE-Juel1)jics40_20190501$ /
                      $G:(DE-Juel1)jics42_20191101$},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32322956},
      UT           = {WOS:000528138600001},
      doi          = {10.1007/s00430-020-00675-1},
      url          = {https://juser.fz-juelich.de/record/886069},
}