Skip to main content


  • Poster presentation
  • Open Access

No impact of IL28B polymorphisms on liver enzymes in patients coinfected with HIV and HCV

  • 1,
  • 2,
  • 2,
  • 2,
  • 2,
  • 2 and
  • 2
Journal of the International AIDS Society201013 (Suppl 4) :P206

  • Published:


  • Liver Fibrosis
  • Elevated Liver Enzyme
  • Prothrombin Activity
  • IL28B Genotype
  • IL28B Polymorphism


IL-28B single nucleotide polymorphisms (SNPs) strongly influence both spontaneous HCV clearance and response to peginterferon-ribavirin therapy. There is no information about the impact of IL28B SNPs on the natural history of HCV liver disease and/or the rate of elevated liver enzymes.


A cohort of HIV/HCV coinfected individuals with normal (<41 IU/L) or elevated (41 IU/L) ALT levels for >12 months were screened for the rs12979860 SNP at the IL-28B gene. The proportion of patients with the favorable (CC) or unfavorable (CT/TT) genotypes were compared in both groups.


A total of 124 patients (44% normal ALT levels, median age 42 years, 68% males, 93% IDUs, 33% alcohol abuse, 5% HBsAg+, median CD4 count 511 cells/µL, median serum HCV-RNA 6.05 log10 copies/mL, 62% HCV genotype 1) were analyzed. Overall 34% of the whole population displayed the IL-28B CC genotype. When comparing ALT groups, 18 (32.7%) with normal ALT showed CC vs 25 (36.2%) with elevated ALT (p=0.71). Using elastometry (FibroScan), liver fibrosis estimates were significantly lower at baseline in patients with normal vs elevated ALT (6.3±2 vs 14.4±12 kPa, respectively, p<0.001). Other differences amongst groups were not significant, as follows: baseline serum HCV-RNA (5.95 vs 6.05 log10 IU/mL, p=0.62), CD4 counts (499 vs 543 cells/µl, p=0.34), and prothrombin activity (91% in both groups, p=0.99). Patients with normal vs elevated ALT were found to be coinfected more frequently with HCV genotypes 1 or 4 (45% vs 26%, p=0.02).


IL28B genotypes do not influence ALT levels in HIV-HCV coinfected patients. Higher ALT levels are associated with a greater extent of liver fibrosis.

Authors’ Affiliations

Hospital Carlos III, Infectious Diseases, Madrid, Spain
Department of Infectious Diseases, Hospital Carlos III, C/ Sinesio Delgado 10, Madrid, Spain


© Fernández-Montero et al; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.