Chromatin, non-coding RNAs, and the expression of HIV

Abstract

HIV is a chronic viral infection affecting an estimated 34 million people worldwide. Current therapies employ the use of a cocktail of antiretroviral medications to reduce the spread and effects of HIV, however complete eradication from an individual currently remains unattainable. Viral latency and regulation of gene expression is a key consideration when developing effective treatments. While our understanding of these processes remains incomplete new developments suggest that non-coding RNA (ncRNA) mediated regulation may provide an avenue to controlling both viral expression and latency. Here we discuss the importance of known regulatory mechanisms and suggest directions for further study, in particular the use ncRNAs in controlling HIV expression.

Figure 1

The LTR promoter of HIV. The genomic organization of HIV-1 is shown with lines emphasizing/delineating the 5' LTR/promoter. The transcription factor AP1, NFAT‑1, IL-2RE, NF-kB, Sp1 and LBP-1 binding sites, TATA box, upstream weak transcriptional start TAGAA, Tat activating region (TAR), and the AAUAA poly‑adenylation sites downstream of TAR in the LTR are shown. Note not all transcription factor binding sites are shown.