HIV-1 Rev Response Element (RRE)

The HIV-1 Rev Response Element (RRE) is a highly structured, approximately 350-nucleotide RNA segment located within the env coding region of the HIV-1 genome [1, 6]. Its primary biological function is to serve as a binding scaffold for the viral Rev protein, which facilitates the nuclear export of unspliced and partially spliced viral mRNAs [1, 9]. This process is essential for the late phase of the HIV-1 life cycle, as it allows the transport of transcripts encoding structural proteins like Gag, Pol, and Env to the cytoplasm for translation and virion assembly [6, 13]. Without the Rev-RRE interaction, these essential transcripts are retained in the nucleus and eventually degraded or spliced, effectively halting viral replication [8, 12]. As a critical regulator of the viral life cycle, the RRE is considered a significant therapeutic target for anti-HIV drug development [1, 2]. Various small molecules, such as benfluron and certain aminoglycosides like neomycin, have been studied for their ability to disrupt the Rev-RRE complex or inhibit Rev oligomerization [4, 7, 8]. Although no RRE-targeting drugs are currently clinically approved, the high conservation of the RRE sequence makes it an attractive site for overcoming drug resistance seen with traditional enzymatic inhibitors [1, 6].

Other names

HIV-1 Rev-dependent RNARev-binding elementRRE RNARev-responsive element

Inhibition of Rev-RRE binding, disruption of Rev oligomerization, and blockade of nuclear export of viral mRNA