There’s nothing restricting miRNAs to targeting just endogenous mRNAs. So it’s no surprise to find that expression of miR-29a – which targets the 3’UTR of HIV-1 mRNA — increases during HIV infection.
Researchers from U Mass Med School in Worchester, and the Burnham Institute for Medical Research in La Jolla, found that HIV mRNA hangs around with RNA-induced silencing complexes (RISCs) and cytoplasmic mRNA-processing-bodies (P bodies) in latently infected cells. Adding in more miR-29a enhances the relationship.
But when they block the action of miR-29a – with antisense oligos, for example – HIV replication goes up. The same thing happens when they disrupt the integrity of the P bodies themselves. So it looks like miR-29a keeps HIV from going postal, which in turn helps it to evade immune detection and eradication by antiviral treatments.
Check out all the details at Molecular Cell, June 2009.