title: Inhibition of translation initiation factors might be the potential therapeutic targets for HCV patients with hepatic iron overload.
abstract: Standard therapy, interferon-alpha (IFN-α) and ribavirin, remains the only available option for treatment of patients with hepatitis C virus (HCV) infection. However, iron overload, a common finding among HCV patients, have a poor response to treatment with current therapy. These data suggest that both host and viral factors are involved in the determination of the outcome of the therapy. Currently, novel antiviral compounds focus on the development of indirect antiviral drugs. The process of the viral translation is considered as the potential therapeutic targets. Coincidentally, study has found that hepatic iron load enhances the levels of eukaryotic initiation factor 3 (eIF3), which is essential for HCV translation. Reversely, iron chelation could reduce eIF3 p170 translation. Our hypothesis is that iron overload may specifically enhance cellular eIFs. As a result, the cellular mechanisms, in patients with iron overload, are utilized for translating viral mRNA into protein. Thus, treatment strategies that target eIFs should be an exceptionally good candidate therapeutic method for HCV patients with hepatic iron overload.
authors: Center of Hygiene Assessment, Institute of Disease Prevention and Control, Academy of Military Medical Sciences, Beijing 100071, China. liuyp31@sina.com.cn
authors: Yiping
authors: Y
authors: Liu
authors: Daizhi
authors: D
authors: An
authors: Rubao
authors: R
authors: Sun
authors: Lianqun
authors: L
authors: Jin
authors: Qiang
authors: Q
authors: Wang
mesh_terms: D039621:Eukaryotic Initiation Factor-3 / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D016174:Hepacivirus / Q000187:drug effects / Q000235:genetics; D006526:Hepatitis C / Q000150:complications* / Q000188:drug therapy; D006801:Humans; D019190:Iron Overload / Q000188:drug therapy* / Q000209:etiology; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008954:Models, Biological; D010455:Peptides / Q000494:pharmacology; D014176:Protein Biosynthesis / Q000187:drug effects / Q000235:genetics
chemical_list: D039621:Eukaryotic Initiation Factor-3; D010455:Peptides