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      DDX1 promotes proliferation of the JC virus through transactivation of its promoter.

      Microbiology and immunology
      Cell Line, Tumor, Cleavage Stimulation Factor, genetics, DEAD-box RNA Helicases, metabolism, Electrophoretic Mobility Shift Assay, methods, Gene Expression Regulation, Viral, Humans, JC Virus, physiology, Polyomavirus Infections, virology, Promoter Regions, Genetic, Transcriptional Activation, Tumor Virus Infections, Virus Replication

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          Abstract

          Recently, we demonstrated that the DEAD box protein 1 (DDX1), an RNA helicase, and the cleavage stimulation factor (CstF) form a complex that binds to the JC virus transcriptional control region (JCV-TCR). Here, we examined the function of DDX1, which is expressed at much higher levels in the JCV-susceptible cell line IMR-32 than in non-susceptible cell lines. DDX1 had no effect on the replication efficiency of JCV, but overexpression of DDX1 significantly increased transactivation of the JCV promoter. Furthermore, DDX1 enhanced the expression of JCV proteins in JCV infected cells, and knockdown of DDX1 using small interfering (si) RNA suppressed the expression of JCV proteins. Our results clearly demonstrate that DDX1 regulates proliferation of JCV in vitro through transcriptional activation.

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