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Farghaly et al. Hepatoma Res 2018;4:41                           Hepatoma Research
               DOI: 10.20517/2394-5079.2018.30




               Original Article                                                              Open Access


               Heat shock reduces HCV replication via regulation
               of ribosomal L22 in Alu-RNA molecule dependent

               manner


               Hamada Farghaly, Adel A. Guirgis, Hany Khalil

               Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat
               City 79, Egypt.

               Correspondence to: Dr. Hany Khalil, Department of Molecular Biology, Genetic Engineering and Biotechnology Research
               Institute, University of Sadat City, Sadat City 79, Egypt. E-mail: hkhalil74@gmail.com

               How to cite this article: Farghaly H, Guirgis AA, Khalil H. Heat shock reduces HCV replication via regulation of ribosomal L22 in
               Alu-RNA molecule dependent manner. Hepatoma Res 2018;4:41. http://dx.doi.org/10.20517/2394-5079.2018.30

               Received: 26 Mar 2018    First Decision: 10 May 2018    Revised: 29 Jun 2018    Accepted: 29 Jun 2018    Published: 7 Aug 2018

               Science Editor: Guang-Wen Cao    Copy Editor: Jun-Yao Li    Production Editor: Cai-Hong Wang


               Abstract
               Aim: Hepatitis C virus (HCV) infection is a global health problem that affects more than 180 million people worldwide.
               HCV is associated with several hepatic and other hepatic disorders including malignancies. HCV is a small enveloped
               positive-single strand RNA virus that belongs to Hepacivirus in the family Flaviviridae. Here we aim to provide a new
               therapeutic strategy via treatment of infected HepG2 cells with heat shock (HS).


               Methods: The potential inhibitory effect of HS on HCV replication was assessed by the relative gene expression of NS5A
               and its corresponding protein by flowcytometry which has been additionally used to monitor other cellular factors.


               Results: HS treatment of infected HepG2 cells has the ability to disturb HCV replication possibly via stimulation of the
               Alu non-coding element which inhibits gene expression of ribosomal L22. Ribosomal protein L22 (RPl22) is one of the
               abundant RNA-binding proteins that are known to facilitate synthesis and translation of viral RNA and to participate in
               balancing the protein components of the ribosome itself.

               Conclusion: HS treatment of infected cells leads to up-regulation of long RNA-Alu molecule that regulates the expression
               of RPL22 and subsequently reduces HCV replication in HepG2 cells.

               Keywords: Hepatitis C virus, Alu non-coding gene, heat shock treatment



                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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