کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6142027 1594334 2016 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
HIV-1 Vpr increases HCV replication through VprBP in cell culture
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ویروس شناسی
پیش نمایش صفحه اول مقاله
HIV-1 Vpr increases HCV replication through VprBP in cell culture
چکیده انگلیسی
Coinfection of human immunodeficiency virus (HIV) and hepatitis C virus (HCV) occurs at a high frequency, in which HIV shows a promotion of HCV-derived liver diseases. However, the mechanism of how this occurs is not well understood. Our previous work has demonstrated that the HIV-1 accessory protein Vpr enhances HCV RNA replication in cell culture. Because Vpr performs most of its functions through host protein VprBP (DCAF1), the role of VprBP in the regulation of HCV by Vpr was investigated in this study. We found that the Vpr mutant Q65R, which is deficient in VprBP binding, could not enhance HCV replication. Furthermore, Vpr-mediated enhancement of HCV replication was severely diminished in VprBP knockdown cells. In addition, an inhibitor of Cullin RING E3 ligases, MLN4924, impaired the function of Vpr during HCV replication. Together, these results suggest that Vpr promotes HCV replication in a VprBP-dependent manner, and that the activity of Cullin RING E3 ligases is essential to this process. In conclusion, our findings demonstrate that HIV-1 Vpr makes the cellular environment more suitable for HCV replication, which might relate with the host ubiquitination system.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Virus Research - Volume 223, 2 September 2016, Pages 153-160
نویسندگان
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