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\datalist[entry]{nyt/global//global/global}
  \entry{saito_innate_2008}{article}{}
    \name{author}{5}{}{%
      {{hash=ST}{%
         family={Saito},
         familyi={S\bibinitperiod},
         given={Takeshi},
         giveni={T\bibinitperiod},
      }}%
      {{hash=ODM}{%
         family={Owen},
         familyi={O\bibinitperiod},
         given={David\bibnamedelima M.},
         giveni={D\bibinitperiod\bibinitdelim M\bibinitperiod},
      }}%
      {{hash=JF}{%
         family={Jiang},
         familyi={J\bibinitperiod},
         given={Fuguo},
         giveni={F\bibinitperiod},
      }}%
      {{hash=MJ}{%
         family={Marcotrigiano},
         familyi={M\bibinitperiod},
         given={Joseph},
         giveni={J\bibinitperiod},
      }}%
      {{hash=GM}{%
         family={Gale},
         familyi={G\bibinitperiod},
         given={Michael},
         giveni={M\bibinitperiod},
      }}%
    }
    \list{language}{1}{%
      {eng}%
    }
    \keyw{Humans, Adenine, Animals, Cell Line, DEAD Box Protein 58, DEAD-box
  RNA Helicases, Genome, Viral, Hepacivirus, Immunity, Innate, Interferon-beta,
  Ligands, Liver, Mice, RNA, Viral, Uridine, Virus Replication}
    \strng{namehash}{ST+1}
    \strng{fullhash}{STODMJFMJGM1}
    \field{labelnamesource}{author}
    \field{labeltitlesource}{title}
    \field{labelyear}{2008}
    \field{labeldatesource}{}
    \field{sortinit}{S}
    \field{sortinithash}{S}
    \field{abstract}{%
    Innate immune defences are essential for the control of virus infection and
  are triggered through host recognition of viral macromolecular motifs known
  as pathogen-associated molecular patterns (PAMPs). Hepatitis C virus (HCV) is
  an RNA virus that replicates in the liver, and infects 200 million people
  worldwide. Infection is regulated by hepatic immune defences triggered by the
  cellular RIG-I helicase. RIG-I binds PAMP RNA and signals interferon
  regulatory factor 3 activation to induce the expression of
  interferon-alpha/beta and antiviral/interferon-stimulated genes (ISGs) that
  limit infection. Here we identify the polyuridine motif of the HCV genome 3'
  non-translated region and its replication intermediate as the PAMP substrate
  of RIG-I, and show that this and similar homopolyuridine or
  homopolyriboadenine motifs present in the genomes of RNA viruses are the
  chief feature of RIG-I recognition and immune triggering in human and murine
  cells. 5' terminal triphosphate on the PAMP RNA was necessary but not
  sufficient for RIG-I binding, which was primarily dependent on homopolymeric
  ribonucleotide composition, linear structure and length. The HCV PAMP RNA
  stimulated RIG-I-dependent signalling to induce a hepatic innate immune
  response in vivo, and triggered interferon and ISG expression to suppress HCV
  infection in vitro. These results provide a conceptual advance by defining
  specific homopolymeric RNA motifs within the genome of HCV and other RNA
  viruses as the PAMP substrate of RIG-I, and demonstrate immunogenic features
  of the PAMP-RIG-I interaction that could be used as an immune adjuvant for
  vaccine and immunotherapy approaches.%
    }
    \verb{doi}
    \verb 10.1038/nature07106
    \endverb
    \field{issn}{1476-4687}
    \field{number}{7203}
    \field{pages}{523\bibrangedash 527}
    \field{title}{Innate immunity induced by composition-dependent {RIG}-{I}
  recognition of hepatitis {C} virus {RNA}}
    \field{volume}{454}
    \verb{file}
    \verb Version acceptée:/home/virginie/snap/zotero-snap/common/Zotero/stora
    \verb ge/K9CLJT9Q/Saito et al. - 2008 - Innate immunity induced by composit
    \verb ion-dependent R.pdf:application/pdf
    \endverb
    \field{journaltitle}{Nature}
    \field{month}{07}
    \field{year}{2008}
  \endentry
\enddatalist
\endinput