Abstract
Retroviruses exploit nuclear trafficking machinery at several distinct stages in their replication cycles. In this review, we will focus primarily on nucleocytoplasmic trafficking events that occur after the completion of reverse transcription and proviral integration. First, we will discuss nuclear export of unspliced viral RNA transcripts, which serves two essential roles: as the mRNA template for the translation of viral structural proteins and as the genome for encapsidation into virions. These full-length viral RNAs must overcome the cell’s quality control measures to leave the nucleus by co-opting host factors or encoding viral proteins to mediate nuclear export of unspliced viral RNAs. Next, we will summarize the most recent findings on the mechanisms of Gag nuclear trafficking and discuss potential roles for nuclear localization of Gag proteins in retrovirus replication.
Highlights
Nuclear Trafficking Events in Retrovirus ReplicationRetroviruses interact with nuclear trafficking machinery during several different phases of their replication cycles (Figure 1)
(matrix), IN, Vpr, and the reverse-transcribed proviral DNA have been implicated in nuclear entry of the pre-integration complex (PIC), more recent data indicate that the CA protein, nuclear import factor transportin-3 (TNPO3), and the nucleoporin Nup358 are important determinants [4,5,6,7,8,9,10,11,12,13,14,15]
Deletion of the sequence caused feline immunodeficiency virus (FIV) RNA to be retained at the nuclear rim, whereas the Gag protein was localized to the plasma membrane
Summary
Retroviruses interact with nuclear trafficking machinery during several different phases of their replication cycles (Figure 1). Productive retroviral infection requires unspliced viral transcripts to be transported into the cytoplasm where they are translated into the essential viral proteins Gag and Gag-Pol. To circumvent intrinsic cellular blockades that prevent the export of incompletely spliced RNAs from the nucleus, complex retroviruses encode trans-acting viral proteins that export their intron-containing viral RNAs from the nucleus. It is intriguing to postulate that Matrin 3 bridges the interaction between Rev and active HIV-1 RNA transcription sites [60,129,135,136], recruiting the CRM1 nuclear export machinery associated with nuclear regulatory networks to transport viral ribonucleoprotein complexes (RNPs) through the nuclear pore and into the cytoplasm
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