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

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

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