Human immunodeficiency virus type 1 Rev–Rev Response Element RNA complex (HIV-1 Rev–RRE complex)

The HIV-1 Rev–Rev Response Element (RRE) RNA complex is a vital ribonucleoprotein assembly essential for the late phase of the Human Immunodeficiency Virus type 1 replication cycle (Pollard & Malim, 1998). The viral Rev protein specifically recognizes and binds to the RRE, a highly structured 350-nucleotide RNA motif located within the env gene of the viral genome (DiMattia et al., 2016). This binding event triggers the multimerization of Rev proteins on the RNA, which subsequently recruits the host nuclear export receptor CRM1 (Exportin-1) to transport unspliced and singly-spliced viral mRNAs from the nucleus to the cytoplasm. Without the formation of this functional complex, essential viral structural proteins such as Gag, Pol, and Env cannot be synthesized, and the viral genome cannot be packaged into new virions. Because this transport mechanism is indispensable for viral propagation and lacks a direct functional analog in healthy human cells, it is a high-priority target for novel antiretroviral drug development (Jayaraman et al., 2022). Current therapeutic strategies focus on small molecules, aptamers, or peptidomimetics that competitively inhibit the Rev-RRE interaction or prevent the assembly of the functional oligomeric complex.

Other names

Rev-RRE complexHIV-1 Rev-RRE interactionRev-response element complexRev-RRE ribonucleoprotein complex

Inhibition of Rev protein binding to the Rev Response Element (RRE) RNA, disruption of Rev oligomerization, or blockade of the CRM1-mediated nuclear export pathway.