HIV infection aggravates the progression of liver damage in HCV-coinfected patients, with the underlying pathogenesis being\nmultifactorial. Although high level of oxidative stress has been observed frequently in patients infected with HIV or HCV, the\nstatus of oxidative stress in HIV/HCV coinfection and its contribution to HCV liver damage have not been determined. This\nstudy involved 363 HBsAg-negative, anti-HCV-positive former blood donors recruited from a village in central China in July\n2005; of these, 140 were positive for HIV. Of these 363 subjects, 282 were successfully followed up through July 2009. HIV/HCVcoinfected\nsubjects had higher rates of end-stage liver disease-related death than those monoinfected with HCV. Liver ultrasound\nmanifestations were poor in HIV-positive than in HIV-negative individuals, in both chronic HCV carriers and those with resolved\nHCV. Serum concentrations of total glutathione (tGSH), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), GSSG, and\nreduced GSH were higher in HIV-positive than HIV-negative subjects. GSSG concentrations were higher in HIV-infected subjects\nwith abnormal ALT/AST levels than in those with normal ALT/AST levels and were associated with poorer liver ultrasound\nmanifestations. These finding indicated that HIV infection accelerated HCV-associated liver damage in HIV/HCV-coinfected\nindividuals. Increased oxidative stress, induced primarily by HIV coinfection, may contribute to aggravated liver damage.
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