Abstract
The cellular metabolism of host tRNAs and life cycle of HIV-1 cross paths at several key virus–host interfaces. Emerging data suggest a multi-faceted interplay between host tRNAs and HIV-1 that plays essential roles, both structural and regulatory, in viral genome replication, genome packaging, and virion biogenesis. HIV-1 not only hijacks host tRNAs and transforms them into obligatory reverse transcription primers but further commandeers tRNAs to regulate the localization of its major structural protein, Gag, via a specific interface. This review highlights recent advances in understanding tRNA–HIV-1 interactions, primarily from a structural perspective, which start to elucidate their underlying molecular mechanisms, intrinsic specificities, and biological significances. Such understanding may provide new avenues toward developing HIV/AIDS treatments and therapeutics including small molecules and RNA biologics that target these host–virus interfaces.
Highlights
Viruses are opportunistic parasitic pathogens that mutate and evolve at accelerated paces compared to their hosts
One of the most abundant and essential components of the host housekeeping machinery is the dynamic pool of transfer RNAs that continually ferry amino acids to the ribosomes to sustain protein synthesis, cellular growth, and renewal
As a primary conduit between the RNA world and the protein world, transfer RNAs (tRNAs) act as physical bridges and adaptors to enable RNA-directed, RNA-catalyzed protein synthesis [1,2,3,4,5,6]. Such pivotal roles of tRNAs in cellular mechanism have subjected them to constant natural selection and evolution. This is evidenced by the high percentage of tRNA nucleotides that receive post-transcriptional modifications compared to mRNAs and even rRNAs, as well as the acquisition, fixation, and propagation of complex protein enzymes dedicated to fine-tuning tRNA structure and functions [7,8,9,10,11,12,13,14,15]
Summary
Viruses are opportunistic parasitic pathogens that mutate and evolve at accelerated paces compared to their hosts. As a primary conduit between the RNA world and the protein world, tRNAs act as physical bridges and adaptors to enable RNA-directed, RNA-catalyzed protein synthesis [1,2,3,4,5,6] Such pivotal roles of tRNAs in cellular mechanism have subjected them to constant natural selection and evolution. Host tRNAs largely exist as abundant, solvent-exposed molecules that feature a well-defined “L”-shaped overall architecture, characteristic molecular and electrostatic surfaces and crevices, and are critically important to sustain the host metabolism These properties together make tRNAs attractive and vulnerable targets to be manipulated and exploited by viruses to serve their own purposes. I discuss recent progress in understanding these viral strategies at the expanding host–virus interfaces between tRNAs and HIV-1, primarily from a structural perspective
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