Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1998-6-12
pubmed:abstractText
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 x 10(5) Eq/mL to 161 x 10(5) 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3841-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9573022-Adult, pubmed-meshheading:9573022-Aged, pubmed-meshheading:9573022-B-Lymphocytes, pubmed-meshheading:9573022-Carrier State, pubmed-meshheading:9573022-Cohort Studies, pubmed-meshheading:9573022-Female, pubmed-meshheading:9573022-Genotype, pubmed-meshheading:9573022-Hepacivirus, pubmed-meshheading:9573022-Hepatitis, Chronic, pubmed-meshheading:9573022-Hepatitis C, pubmed-meshheading:9573022-Humans, pubmed-meshheading:9573022-Macrophages, pubmed-meshheading:9573022-Male, pubmed-meshheading:9573022-Middle Aged, pubmed-meshheading:9573022-Monocytes, pubmed-meshheading:9573022-Neutrophils, pubmed-meshheading:9573022-Phagocytosis, pubmed-meshheading:9573022-Phenotype, pubmed-meshheading:9573022-Polymerase Chain Reaction, pubmed-meshheading:9573022-RNA, Viral, pubmed-meshheading:9573022-Sensitivity and Specificity, pubmed-meshheading:9573022-T-Lymphocytes, pubmed-meshheading:9573022-Viremia, pubmed-meshheading:9573022-Virus Replication
pubmed:year
1998
pubmed:articleTitle
In vivo tropism of hepatitis C virus genomic sequences in hematopoietic cells: influence of viral load, viral genotype, and cell phenotype.
pubmed:affiliation
INSERM U271, Lyon, France.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't