Role of nucleocytoplasmic RNA transport during the life cycle of retroviruses
- Division of Molecular Virology, Institute of Immunological Science, Hokkaido University, Sapporo, Japan
Retroviruses have evolved mechanisms for transporting their intron-containing RNAs (including genomic and messenger RNAs, which encode virion components) from the nucleus to the cytoplasm of the infected cell. Human retroviruses, such as human immunodeficiency virus (HIV) and human T cell leukemia virus type 1 (HTLV-1), encode the regulatory proteins Rev and Rex, which form a bridge between the viral RNA and the export receptor CRM1. Recent studies show that these transport systems are not only involved in RNA export, but also in the encapsidation of genomic RNA; furthermore, they influence subsequent events in the cytoplasm, including the translation of the cognate mRNA, transport of Gag proteins to the plasma membrane, and the formation of virus particles. Moreover, the mode of interaction between the viral and cellular RNA transport machinery underlies the species-specific propagation of HIV-1 and HTLV-1, forming the basis for constructing animal models of infection. This review article discusses recent progress regarding these issues.
Keywords: RNA export, HTLV-1, HIV-1, infection rat models for, CRM1, simple retrovirus, species-specific barrier, Rex/Rev
Citation: Shida H (2012) Role of nucleocytoplasmic RNA transport during the life cycle of retroviruses. Front. Microbio. 3:179. doi: 10.3389/fmicb.2012.00179
Received: 26 March 2012; Paper pending published: 16 April 2012;
Accepted: 26 April 2012; Published online: 18 May 2012.
Edited by:Atsushi Koito, Kumamoto University, Japan
Reviewed by:Yasuo Ariumi, Kumamoto University, Japan
Tominori Kimura, Ritsumeikan University, Japan
Copyright: © 2012 Shida. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
*Correspondence: Hisatoshi Shida, Division of Molecular Virology, Institute of Immunological Science, Hokkaido University, Sapporo 060-0815, Japan. e-mail: firstname.lastname@example.org