Abstract
To replicate and disseminate, viruses need to manipulate and modify the cellular machinery for their own benefit. We are interested in translation, which is one of the key steps of gene expression and viruses that have developed several strategies to hijack the ribosomal complex. The type 1 human immunodeficiency virus is a good paradigm to understand the great diversity of translational control. Indeed, scanning, leaky scanning, internal ribosome entry sites, and adenosine methylation are used by ribosomes to translate spliced and unspliced HIV-1 mRNAs, and some require specific cellular factors, such as the DDX3 helicase, that mediate mRNA export and translation. In addition, some viral and cellular proteins, including the HIV-1 Tat protein, also regulate protein synthesis through targeting the protein kinase PKR, which once activated, is able to phosphorylate the eukaryotic translation initiation factor eIF2α, which results in the inhibition of cellular mRNAs translation. Finally, the infection alters the integrity of several cellular proteins, including initiation factors, that directly or indirectly regulates translation events. In this review, we will provide a global overview of the current situation of how the HIV-1 mRNAs interact with the host cellular environment to produce viral proteins.
Highlights
Flexibility and adaptability are both essentials when facing difficult situations; such an assumption retains all its meaning when it comes to the viral kingdom
We have shown that DDX3 interacts with the trans-activation response (TAR) stem loop and with regions of the 5 UTR IRES [141], and this characteristic opens the possibility that DDX3 may participate in IRES-mediated initiation
In contrast to other viruses, such as Hepatitis C virus (HCV), EMCV, or poliovirus, for which translation relies exclusively on IRES-mediated initiation, the unspliced HIV-1 genomic RNA can use three different mechanisms of ribosomal recruitment: (i) Similar to cellular messenger RNAs (mRNAs), ribosome attachment can occur at the cap structure and it requires different RNA helicases (RHA, DDX3, La, and TAR RNA binding protein (TRBP)) to promote unwinding of the 5 end TAR structure
Summary
Flexibility and adaptability are both essentials when facing difficult situations; such an assumption retains all its meaning when it comes to the viral kingdom. The type 1 human immunodeficiency virus (HIV-1) is a member of the Lentivirus genus from the Retroviridae family and the etiologic agent of the acquired immunodeficiency syndrome. It is a good representative of this viral adaptability with more than 50 viral RNA transcripts produced by alternative splicing [1,2,3] that allow for the expression of 15 proteins [4]. We will focus on the unspliced genomic RNA Translation of this transcript can use both a classical translation initiation mechanism and internal recruitment of ribosomes in order to adapt to the cellular modifications imposed by infection
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