Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-11-5
pubmed:abstractText
Hepatitis C virus (HCV)/human immunodeficiency virus (HIV) coinfection poses a difficult therapeutic problem. Response to HCV-specific therapy is variable but might be influenced by host genetic factors, including polymorphisms of cytokine genes. Here, we studied whether interleukin-6 (IL-6) C174G gene polymorphism affects the response to antiviral treatment in HCV-infected HIV-positive subjects. We determined IL-6 genotypes in HIV-positive patients with acute (n = 52) and chronic (n = 60) hepatitis C treated with pegylated interferon-alpha. Two hundred ten HCV monoinfected, 197 HIV monoinfected, and 100 healthy individuals were studied as controls. Patients were classified into high and low producers according to IL-6 genotypes. Rates of sustained virological responses (SVRs) were compared between the IL-6 genotypes. Signal transducer and activator of transcription three phosphorylation was analyzed by Western blot in HCV core-transfected human hepatoma cell line (HUH7) cells. Distribution of IL-6 genotypes did not differ significantly between the study groups. SVR was achieved in 63% of HIV/HCV coinfected patients. Carriers of the IL-6 high producer (HP) genotype had significantly higher SVR rates than patients with an IL-6 low producer genotype (70.1% versus 52%; P < 0.002). This effect was seen in both HIV-positive patients with acute (74% versus 33%; P < 0.05) and chronic (66% versus 33%; P < 0.05) hepatitis C. Multivariate analysis confirmed IL-6 HP carriage as an independent positive predictor for SVR (Odd's ratio 6.1; P = 0.004). This effect corresponds to the in vitro observation that in HCV core-transfected HUH7 cells, IL-6 overcomes the HCV core-mediated inhibition of STAT3 activation. CONCLUSION: Response rates to HCV-specific treatment are higher in HCV/HIV-positive patients carrying the IL-6 HP genotype, which might be because of IL-6 mediated STAT3 activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1016-25
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:17668881-Acute Disease, pubmed-meshheading:17668881-Adult, pubmed-meshheading:17668881-Aged, pubmed-meshheading:17668881-Antiviral Agents, pubmed-meshheading:17668881-Cell Line, Tumor, pubmed-meshheading:17668881-Chronic Disease, pubmed-meshheading:17668881-Dose-Response Relationship, Drug, pubmed-meshheading:17668881-Drug Therapy, Combination, pubmed-meshheading:17668881-Female, pubmed-meshheading:17668881-Genotype, pubmed-meshheading:17668881-HIV Infections, pubmed-meshheading:17668881-Hepatitis C, pubmed-meshheading:17668881-Humans, pubmed-meshheading:17668881-Interferon-alpha, pubmed-meshheading:17668881-Interleukin-6, pubmed-meshheading:17668881-Male, pubmed-meshheading:17668881-Middle Aged, pubmed-meshheading:17668881-Polyethylene Glycols, pubmed-meshheading:17668881-Polymorphism, Single Nucleotide, pubmed-meshheading:17668881-Recombinant Proteins, pubmed-meshheading:17668881-Ribavirin, pubmed-meshheading:17668881-STAT3 Transcription Factor, pubmed-meshheading:17668881-Treatment Outcome
pubmed:year
2007
pubmed:articleTitle
Effect of the interleukin-6 C174G gene polymorphism on treatment of acute and chronic hepatitis C in human immunodeficiency virus coinfected patients.
pubmed:affiliation
Department of Internal Medicine I, University of Bonn, Bonn, Germany. Jacob.Nattermann@ukb.uni-bonn.de
pubmed:publicationType
Journal Article, Controlled Clinical Trial, Research Support, Non-U.S. Gov't