How Do Viruses Avoid Inhibition by Endogenous Cellular MicroRNAs?

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Analysis of RISC binding to the HIV-1 genome indeed identified several binding sites that were occupied by RISCs programmed by endogenous cellular miRNAs and some of these could be shown, by indicator assays, to confer a modest repression of mRNA function [27]. However, perhaps the more interesting finding was that viral mRNAs, despite contributing more than 10% of the total mRNA transcriptome in HIV-1 infected cells, in fact gave rise to only approximately 0.2% of all assignable RISC binding sites, with the remaining approximately 99.8% being contributed by cellular mRNAs. That is, viral mRNAs are, at a minimum, 50-fold less likely to bind RISC than are cellular mRNAs, consistent with the idea that HIV-1-encoded mRNAs, at least, have evolved to globally avoid cellular miRNAs by adopting RNA secondary structures that preclude RISC binding.

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