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Prepublished online as a Blood First Edition Paper on June 28, 2002; DOI 10.1182/blood-2002-03-0818.
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Blood, 1 January 2003, Vol. 101, No. 1, pp. 52-57
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Differential distribution and internal translation efficiency of
hepatitis C virus quasispecies present in dendritic and liver
cells
Julien Laporte,
Christine Bain,
Patrick Maurel,
Genevieve Inchauspe,
Henri Agut, and
Annie Cahour
From the Laboratoire de virologie, C.E.R.VI., UPRES EA
2387, Hôpital Pitié-Salpêtrière, Paris,
France; Unité Mixte CNRS-bioMérieux, Ecole
Normale Supérieure, Lyon, France; INSERM U128, CNRS,
BP5051, Montpellier, France.
Hepatitis C virus (HCV) is predominantly a hepatotropic virus.
Nonetheless, there is mounting evidence that hematopoietic cells may
support HCV replication. The HCV 5' untranslated region (5'UTR),
responsible for initiation of viral translation, via an internal
ribosome entry site (IRES), has been previously described to contain
specific nucleotide substitutions when cultured in infected lymphoid
cells. Our purpose was to establish whether the 5'UTR polymorphism of
quasispecies from 3 cell compartments (liver, peripheral blood
mononuclear cells [PBMG], and monocyte-derived dendritic cells
[DCs]) of a patient chronically infected with HCV1b affects the
corresponding translational efficiencies and thus the capacity for
replication. The 5'UTR polymorphism was characterized by identification
of changes at 3 crucial sites as compared with the reference nucleotide
(nt) sequence: a G insertion between positions 19 and 20, a C>A
substitution at position 204 and a G>A substitution at position 243. The quasispecies detected in DCs was unique and differed from those
present in the liver, suggesting a particular tropism of HCV
quasispecies for DCs. Moreover, its translational activity was
significantly impaired when compared with those from liver and PBMCs in
different cell lines. This impairment was thoroughly confirmed in
primary cultures of both human hepatocytes and monocyte-derived DCs.
Taken together, our data lend support both to a specific location and
impaired replication of HCV quasispecies in DCs, which could be related
to viral persistence and perturbation of DC function in chronically
infected patients.
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