Response to pegylated interferon-α 2a plus ribavirin of 267 HIV/HCV coinfected patients, grouped as a function of HCV genotype.

<p>Data are shown as absolute number (percentage).</p

Characteristics of HIV-HCV coinfected patients treated with pegylated interferon-α 2a plus ribavirin (n = 267), grouped as a function of HCV genotype and presence or absence of sustained virological response.

<p>Abbreviations: SNP: Single nucleotide polymorphism. RVR: Rapid virologic response. ETR: Virologic response at the end of treatment. SVR: Sustained virologic response.</p

Percentages of HIV/HCV coinfected patients (HCV genotype 1) with rapid (lined) and sustained (black) virological response to pegylated interferon-α 2a plus ribavirin as a function of IL28B polymorphism and HCV-RNA levels.

<p>Percentages of HIV/HCV coinfected patients (HCV genotype 1) with rapid (lined) and sustained (black) virological response to pegylated interferon-α 2a plus ribavirin as a function of IL28B polymorphism and HCV-RNA levels.</p

Multivariant analysis of factors associated with the development of liver cirrhosis in HIV-HCV coinfected patients.

<p>Multivariant analysis of factors associated with the development of liver cirrhosis in HIV-HCV coinfected patients.</p

Serum concentrations of tumor necrosis factor-α (TNF-α) (white bars), interleukins 6 (IL-6) (lined bars) and 10 (IL-10) (dotted bars) and transforming growth factor beta 1 (TGF-β1) (black bars) in healthy controls (A) and in HIV-HCV coinfected patients with chronic hepatits (B) (n = 50) or liver cirrhosis (C) in function of the polymorphisms of -238 and -308 TNF-α and -592 IL-10 promotor genes.

<p>Serum concentrations of tumor necrosis factor-α (TNF-α) (white bars), interleukins 6 (IL-6) (lined bars) and 10 (IL-10) (dotted bars) and transforming growth factor beta 1 (TGF-β1) (black bars) in healthy controls (A) and in HIV-HCV coinfected patients with chronic hepatits (B) (n = 50) or liver cirrhosis (C) in function of the polymorphisms of -238 and -308 TNF-α and -592 IL-10 promotor genes.</p

Percentages of HIV/HCV coinfected patients with sustained virological response to pegylated interferon-α 2a plus ribavirin as a function of IL28B polymorphism, HCV-RNA levels and presence (black) or absence (white) of significant liver fibrosis.

<p>Percentages of HIV/HCV coinfected patients with sustained virological response to pegylated interferon-α 2a plus ribavirin as a function of IL28B polymorphism, HCV-RNA levels and presence (black) or absence (white) of significant liver fibrosis.</p

Characteristics of HIV-infected patients coinfected by HCV genotype 1 treated with pegylated interferon alpha 2a plus ribavirin (n = 187), grouped as a function of the presence or absence of rapid virological response.

<p>Abbreviations: SNP: Single nucleotide polymorphism. RVR: Rapid virologic response. ETR: Virologic response at the end of treatment. SVR: Sustained virologic response.</p

Kaplan Meier curves of the development of liver cirrosis in HIV-HCV patients in function of the polymorphism at -238 position of the TNF-α promoter gene.

<p>Kaplan Meier curves of the development of liver cirrosis in HIV-HCV patients in function of the polymorphism at -238 position of the TNF-α promoter gene.</p

Intracellular expression of tumor necrosis factor alpha, interleukin 6, transforming growth factor beta1 and interleukin 10 by monocytes from healthy individuals distributed in function of the -238 promotor gene polymorphism.

<p>Basal and LPS-stimulated concentration of tumor necrosis factor alpha, interleukin 6, transforming growth factor beta1 and interleukin 10 on supernatants of monocyte cultures. Abbreviations: TNF-α tumor necrosis factor alpha. IL-6, interleukin 6. TGF-β1, transforming growth factor beta 1. IL-10, interleukin 10. LPS, lipopolysaccharide.</p

Single nucleotide polymorphism of TNF-α and IL-10 genes studied in healthy controls and patients with HIV-HCV coinfection.

<p>Note: In Genotype frequency, “n” expresses the number of patients in which the analysis of each polymorphism was successful. By that, it could be no coincidence among the sum of genotype frequencies and the absolute number of patients.</p