Viruses 2016, 8(3), 58; doi:10.3390/v8030058
HTLV-1 Rex Tunes the Cellular Environment Favorable for Viral Replication
Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1, Shirokanedai, Minatoku, Tokyo 108-8639, Japan
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Author to whom correspondence should be addressed.
Academic Editor: Louis M. Mansky
Received: 9 November 2015 / Revised: 9 February 2016 / Accepted: 9 February 2016 / Published: 24 February 2016
(This article belongs to the Special Issue Recent Advances in HTLV Research 2015)
Abstract
Human T-cell leukemia virus type-1 (HTLV-1) Rex is a viral RNA binding protein. The most important and well-known function of Rex is stabilizing and exporting viral mRNAs from the nucleus, particularly for unspliced/partially-spliced mRNAs encoding the structural proteins essential for viral replication. Without Rex, these unspliced viral mRNAs would otherwise be completely spliced. Therefore, Rex is vital for the translation of structural proteins and the stabilization of viral genomic RNA and, thus, for viral replication. Rex schedules the period of extensive viral replication and suppression to enter latency. Although the importance of Rex in the viral life-cycle is well understood, the underlying molecular mechanism of how Rex achieves its function has not been clarified. For example, how does Rex protect unspliced/partially-spliced viral mRNAs from the host cellular splicing machinery? How does Rex protect viral mRNAs, antigenic to eukaryotic cells, from cellular mRNA surveillance mechanisms? Here we will discuss these mechanisms, which explain the function of Rex as an organizer of HTLV-1 expression based on previously and recently discovered aspects of Rex. We also focus on the potential influence of Rex on the homeostasis of the infected cell and how it can exert its function. View Full-TextKeywords:
HTLV-1 Rex; pro-viral expression; unspliced RNA; NMD; alternative splicing; cell cycle regulation
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Nakano, K.; Watanabe, T. HTLV-1 Rex Tunes the Cellular Environment Favorable for Viral Replication. Viruses 2016, 8, 58.
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