title: Liver Damage in Patients with HCV/HIV Coinfection Is Linked to HIV-Related Oxidative Stress.
abstract: HIV infection aggravates the progression of liver damage in HCV-coinfected patients, with the underlying pathogenesis being multifactorial. Although high level of oxidative stress has been observed frequently in patients infected with HIV or HCV, the status of oxidative stress in HIV/HCV coinfection and its contribution to HCV liver damage have not been determined. This study involved 363 HBsAg-negative, anti-HCV-positive former blood donors recruited from a village in central China in July 2005; of these, 140 were positive for HIV. Of these 363 subjects, 282 were successfully followed up through July 2009. HIV/HCV-coinfected subjects had higher rates of end-stage liver disease-related death than those monoinfected with HCV. Liver ultrasound manifestations were poor in HIV-positive than in HIV-negative individuals, in both chronic HCV carriers and those with resolved HCV. Serum concentrations of total glutathione (tGSH), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), GSSG, and reduced GSH were higher in HIV-positive than HIV-negative subjects. GSSG concentrations were higher in HIV-infected subjects with abnormal ALT/AST levels than in those with normal ALT/AST levels and were associated with poorer liver ultrasound manifestations. These finding indicated that HIV infection accelerated HCV-associated liver damage in HIV/HCV-coinfected individuals. Increased oxidative stress, induced primarily by HIV coinfection, may contribute to aggravated liver damage.
authors.affiliation: Department of Microbiology & Infectious Disease Center, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
authors.forename: Xiangbo
authors.initials: X
authors.lastname: Huang
authors.affiliation: State Key Laboratory of Infectious Disease Prevention and Control, National Center for AIDS/STD Control and Prevention, China CDC, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Beijing 102206, China.
authors.forename: Hua
authors.initials: H
authors.lastname: Liang
authors.affiliation: Department of Microbiology & Infectious Disease Center, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
authors.forename: Xueying
authors.initials: X
authors.lastname: Fan
authors.affiliation: Department of Microbiology & Infectious Disease Center, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
authors.forename: Liyan
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Department of Microbiology & Infectious Disease Center, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Shen
mesh_terms: D000328:Adult; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D002681:China; D060085:Coinfection / Q000821:virology; D018450:Disease Progression; D005260:Female; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D015658:HIV Infections / Q000150:complications*; D006526:Hepatitis C / Q000150:complications*; D006801:Humans; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000378:metabolism; D008107:Liver Diseases / Q000000981:diagnostic imaging / Q000473:pathology* / Q000821:virology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008875:Middle Aged; D018384:Oxidative Stress
chemical_list: D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D005978:Glutathione