title: HIV coinfection and antiretroviral therapy enhances liver steatosis in patients with hepatitis C, but only in those infected by HCV genotype other than 3.
abstract: BACKGROUND
  Liver steatosis is a common finding in hepatitis C virus (HCV) infection and is associated with an increased progression of the disease. However, HCV genotype 3 steatosis presents a peculiar and virus-induced pathogenesis. We analysed the effect of HIV coinfection and antiretroviral therapy on hepatic steatosis and the effect of the steatosis on fibrosis in patients with or without HCV genotype 3 infection.
  
  
  METHODS
  All consecutive HIV-infected and uninfected patients who had undergone a liver biopsy for evaluation of HCV infection at the Infectious Diseases Clinic (Modena, Italy) were included in this study. Primary outcomes were the presence or absence of steatosis or the presence of moderate or advanced fibrosis.
  
  
  RESULTS
  A total of 284 patients were enrolled: 187 infected by HCV and 97 coinfected with HIV and HCV. In HCV genotype 3 patients, only HCV-related variables, such as plasma HCV RNA levels (odds ratio [OR] per log10 1.68, P < 0.001) and estimated duration of HCV infection (OR per year 1.17, P = 0.004) were associated with steatosis. In patients infected with other HCV genotypes, steatosis was associated with older age (OR per 5 years 1.47, P < 0.001), with exposure to d-drugs in HIV-HCV-coinfected patients (OR 2.60, P = 0.04) and specifically exposure to stavudine (OR 2.76 HIV-HCV-coinfected versus not HIV-infected patients, P = 0.04). Steatosis was independently associated with bridging fibrosis only in patients infected by HCV genotype other than 3 (OR 4.03, P = 0.01).
  
  
  CONCLUSIONS
  Hepatic steatosis, in both HCV-monoinfected and in HIV-HCV-coinfected patients, is strongly correlated with HCV genotype 3, probably through interactions between HCV virus and liver cells. HIV-related increase of steatosis in patients with HCV is probably related to antiretroviral drugs, especially stavudine, in patients infected by HCV genotype other than 3.
authors.affiliation: Clinic of Infectious and Tropical Diseases, University of Modena and Reggio Emilia, Modena, Italy. borghiv@unimo.it
authors.forename: Vanni
authors.initials: V
authors.lastname: Borghi
authors.forename: Massimo
authors.initials: M
authors.lastname: Puoti
authors.forename: Cristina
authors.initials: C
authors.lastname: Mussini
authors.forename: Stefania
authors.initials: S
authors.lastname: Bellelli
authors.forename: Claudio
authors.initials: C
authors.lastname: Angeletti
authors.forename: Francesca
authors.initials: F
authors.lastname: Sabbatini
authors.forename: Francesca
authors.initials: F
authors.lastname: Prati
authors.forename: Andrea
authors.initials: A
authors.lastname: Cossarizza
authors.forename: Roberto
authors.initials: R
authors.lastname: Esposito
mesh_terms: D000328:Adult; D044966:Anti-Retroviral Agents / Q000009:adverse effects; D005234:Fatty Liver / Q000139:chemically induced / Q000150:complications*; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000150:complications*; D016174:Hepacivirus / Q000235:genetics*; D006526:Hepatitis C / Q000150:complications* / Q000821:virology; D006801:Humans; D016015:Logistic Models; D008297:Male; D016017:Odds Ratio; D012307:Risk Factors
chemical_list: D044966:Anti-Retroviral Agents