Exogenous human immunodeficiency virus-1 protein, tat, enhances replication of JC virus efficiently in neuroblastoma cell lines
Version of Record online: 15 FEB 2012
Copyright © 2012 Wiley Periodicals, Inc.
Journal of Medical Virology
Volume 84, Issue 4, pages 555–561, April 2012
How to Cite
Nukuzuma, S., Kameoka, M., Sugiura, S., Nakamichi, K., Nukuzuma, C., Miyoshi, I. and Takegami, T. (2012), Exogenous human immunodeficiency virus-1 protein, tat, enhances replication of JC virus efficiently in neuroblastoma cell lines. J. Med. Virol., 84: 555–561. doi: 10.1002/jmv.23239
- Issue online: 15 FEB 2012
- Version of Record online: 15 FEB 2012
- Manuscript Accepted: 22 DEC 2011
- The Research Committee of Prion Disease and Slow Virus Infection, the Ministry of Health, Labor and Welfare of Japan
- The High-Tech Center of Kanazawa Medical University. Grant Number: H2011-10
- PML-type JCV;
- HIV-1 Tat protein;
The high incidence of progressive multifocal leukoencephalopathy (PML) among individuals with acquired immunodeficiency syndrome (AIDS) is similar to the incidence of other immunocompromised diseases. The pathogenic JC virus (JCV) with rearranged regulatory regions (PML-type) causes PML, a demyelinating disease in the brains of immunocompromised patients. In a previous study, Tat protein, encoded by human immunodeficiency virus type 1 (HIV-1), markedly enhanced the expression of a reporter gene under control of the JCV late promoter. In order to examine the enhancement of JCV replication by Tat protein, the neuroblastoma cell line IMR-32 was used because it enables IMR-32-adapted JCV. The extent of JCV replication in IMR-32 cells treated with Tat protein was significantly higher than that in untreated IMR-32 cells. The enhancement of JCV propagation by Tat protein was also examined using IMR-32-derived JCV producing (JCI) cells which continuously produce JCV. Treatment of JCI cells with Tat protein led to a significant increase in the titers of progeny viruses. It has also been shown that Tat protein leads to a decrease in the expression of purine-rich element binding protein α (Purα) as an important mediator of JCV replication in IMR-32 cells. Thus, it is probable that Tat protein enhances JCV replication in IMR-32 cells via the down-regulation of Purα expression and cell proliferation. To our knowledge, this is the first report that exogenous Tat protein enhances the replication of JCV efficiently in neuroblastoma cell lines. J. Med. Virol. 84:555–561, 2012. © 2011 Wiley Periodicals, Inc.