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In Vivo Tropism of Hepatitis C Virus Genomic Sequences in
Hematopoietic Cells: Influence of Viral Load, Viral Genotype, and Cell
Phenotype
Hervé Lerat,
Sylvie Rumin,
François Habersetzer,
Françoise Berby,
Mary-Anne Trabaud,
Christian Trépo, and
Geneviève Inchauspé
From INSERM U271, Lyon, France.
Extrahepatic sites capable of supporting hepatitis C virus (HCV)
replication have been suggested. We analyzed the influence of
virological factors such as viral genotype and viral load, and cellular
factors such as cell phenotype, on the detection rate of HCV sequences
in hematopoietic cells of infected patients. Thirty-eight chronically
infected patients were included in the study: 19 infected by genotype 1 isolates (1a and 1b), 13 by nongenotype 1 isolates (including genotypes
2 a/c, 3a, and 4), and 6 coinfected by genotype 1 and 6 isolates.
Polymerase chain reaction (PCR) detection efficiency of viral genomic
sequences, both the positive and negative strand RNA, was evaluated
using RNA transcripts derived from genotype 1, 2, 3, and 4 cloned
sequences and found to be equivalent within one log unit. The serum
viral load, ranging from less than 2 × 105 Eq/mL to 161 × 105 Eq/mL, did not influence the detection rate of
either strand of RNA in patients' peripheral blood mononuclear cells
(PBMCs). Positive and negative strand RNA were found in PBMCs of all 3 cohorts of patients with a detection rate ranging from 15% to 100%
and from 8% to 83.3% for the positive and negative strand RNA,
respectively. Coinfected patients showed a detection rate in all cases
greater than 80%. Patients infected with genotype 1 isolates showed a
higher detection rate of either strands of RNA when compared with
patients infected with other genotypes (P < .001 and
P < .04). Both strands were found restricted to polymorphonuclear leukocytes, monocytes/macrophages, and B (but not T)
lymphocytes. These data show that HCV genomic sequences, possibly
reflecting viral replication, can be detected in PBMCs of chronically
infected patients independent of the viral load and that specific
associated cell subsets are implicated in the harboring of such
sequences.
Blood, Vol. 91 No. 10 (May 15), 1998:
pp. 3841-3849
© 1998 by The American Society of Hematology.
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