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This Article Full Text Full Text (PDF) All Versions of this Article: vir.0.013433-0v1 90/12/2893    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Agis-Juárez, R. A. Articles by del Angel, R. M. PubMed PubMed Citation Articles by Agis-Juárez, R. A. Articles by del Angel, R. M. Agricola Articles by Agis-Juárez, R. A. Articles by del Angel, R. M.

Polypyrimidine tract-binding protein is relocated to the cytoplasm and is required during dengue virus infection in Vero cells

Takiko Daikoku^3,

R. Padmanabhan^3,

¹ Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, Mexico City 07360, Mexico
² Core Laboratory, Centro de Investigación y de Estudios Avanzados del IPN, Mexico City 07360, Mexico
³ University of Kansas Medical Center, USA

Correspondence
Rosa M. del Angel
rmangel{at}cinvestav.mx

The 3' untranslated region (3'UTR) of the dengue virus (DENV) genome contain several sequences required for translation, replication and cyclization processes. This region also binds cellular proteins such as La, polypyrimidine tract-binding protein (PTB), Y box-binding protein 1, poly(A)-binding protein and the translation initiation factor eEF-1. PTB is a cellular protein that interacts with the regulatory sequences of positive-strand RNA viruses such as several picornaviruses and hepatitis C virus. In the present report, it was demonstrated that PTB translocates from the nucleus to the cytoplasm during DENV infection. At 48 h post-infection, PTB, as well as the DENV proteins NS1 and NS3, were found to co-localize with the endoplasmic reticulum marker calnexin. Silencing of PTB expression inhibited virus translation and replication, whilst overexpression of PTB augmented these processes. Thus, these results provide evidence that, during infection, PTB moves from the nucleus to the cytoplasm and plays an important role in the DENV replicative cycle.

Present address: Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA.

Present address: Department of Microbiology and Immunology, Georgetown University, Washington, DC 20057, USA.