title: Progression of liver fibrosis in HIV/HCV genotype 1 co-infected patients is related to the T allele of the rs12979860 polymorphism of the IL28B gene.
abstract: OBJECTIVE
  HIV/HCV co-infection is characterised by accelerated progression of liver disease. Recently, the rs12979860 C/T polymorphism in the IL28B gene has been linked to progression towards cirrhosis in HCV mono-infected patients and to treatment response of HCV-infection in HIV/HCV co-infected patients. Our aim was to clarify by non-invasive techniques if this polymorphism affects fibrosis progression in HIV/HCV co-infection.
  
  
  METHODS
  In a cross-sectional design, liver stiffness (transient elastography), surrogate markers of liver fibrosis (APRI and FIB-4 scores) and rs12979860 genotypes were analysed in 84 HCV/HIV co-infected patients. IL28B genotypes were determined by real-time PCR using a light cycler. In 56 HIV/HCV co-infected patients we also studied progression of fibrosis in relation to rs12979860 C/T genotypes over two years.
  
  
  RESULTS
  82% of the patients were on HAART (74% without detectable HI viremia) and 67% were haemophiliacs, respectively. HCV genotype 1 was present in 62%. Cross-sectional median liver stiffness was 7.4 kPa and correlated with APRI and FIB-4 scores (r = 0.6 each, p < 0.001). Frequencies of IL28B genotypes were: CC 50%, CT 43% and TT 7%. In the cross-sectional analysis liver stiffness values were not different between the various IL28B-genotypes. Upon follow-up under HAART carriers of a C allele did not show further progression, while liver stiffness significantly increased in HIV/HCV co-infected patients with the T allele (p = 0.047).
  
  
  CONCLUSIONS
  Although progression of liver fibrosis was low under HAART in our cohort, progression was more pronounced in HIV/HCV genotype 1 co-infected patients with the T allele.
authors.affiliation: Department of Internal Medicine I, University Hospital Bonn, Sigmund Freud Str. 25, 53105 Bonn, Germany.
authors.forename: P
authors.initials: P
authors.lastname: Lutz
authors.forename: J-C
authors.initials: JC
authors.lastname: Wasmuth
authors.forename: H-D
authors.initials: HD
authors.lastname: Nischalke
authors.forename: N
authors.initials: N
authors.lastname: Vidovic
authors.forename: F
authors.initials: F
authors.lastname: Grünhage
authors.forename: F
authors.initials: F
authors.lastname: Lammert
authors.forename: J
authors.initials: J
authors.lastname: Oldenburg
authors.forename: J K
authors.initials: JK
authors.lastname: Rockstroh
authors.forename: T
authors.initials: T
authors.lastname: Sauerbruch
authors.forename: Ulrich
authors.initials: U
authors.lastname: Spengler
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D023241:Antiretroviral Therapy, Highly Active; D003430:Cross-Sectional Studies; D018450:Disease Progression; D054459:Elasticity Imaging Techniques / Q000379:methods; D005260:Female; D005355:Fibrosis / Q000821:virology*; D005838:Genotype; D006678:HIV / Q000235:genetics*; D015658:HIV Infections / Q000150:complications / Q000821:virology; D016174:Hepacivirus / Q000235:genetics*; D006801:Humans; D007372:Interferons; D007378:Interleukins / Q000235:genetics*; D008107:Liver Diseases / Q000150:complications / Q000821:virology; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D000095022:Interferon Lambda
chemical_list: D007372:Interferons; D007378:Interleukins; C000624353:interferon-lambda, human; D000095022:Interferon Lambda