Kaitao Zhao
Yongxuan Yao
Jing Guo
Xiaoxiao Gao
Qi Yang
Min Guo
Wandi Zhu
Yun Wang
Chunchen Wu
Jizheng Chen
Yuan Zhou
Xue Hu
Mengji Lu
Xinwen Chen
Rongjuan Pei
1 State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China;
2 University of Chinese Academy of Sciences, Beijing 100049, China;
3 Department of Infectious Disease, University Hospital Essen, University of Duisburg-Essen, Gebäude V15, 45117 Essen, Germany
Abstract
Abstract
The secondary structures of hepatitis C virus (HCV) RNA and the cellular proteins that bind to them are important for modulating both translation and RNA replication. However, the sets of RNA-binding proteins involved in the regulation of HCV translation, replication and encapsidation remain unknown. Here, we identified RNA binding motif protein 24 (RBM24) as a host factor participated in HCV translation and replication. Knockdown of RBM24 reduced HCV propagation in Huh7.5.1 cells. An enhanced translation and delayed RNA synthesis during the early phase of infection was observed in RBM24 silencing cells. However, both overexpression of RBM24 and recombinant human RBM24 protein suppressed HCV IRES-mediated translation. Further analysis revealed that the assembly of the 80S ribosome on the HCV IRES was interrupted by RBM24 protein through binding to the 5'-UTR. RBM24 could also interact with HCV Core and enhance the interaction of Core and 5'-UTR, which suppresses the expression of HCV. Moreover, RBM24 enhanced the interaction between the 5'-and 3'-UTRs in the HCV genome, which probably explained its requirement in HCV genome replication. Therefore, RBM24 is a novel host factor involved in HCV replication and may function at the switch from translation to replication.Keywords: RNA binding protein, RBM24, hepatitis C virus, translation, replication
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