Using 2'-O-methylated antisense oligonucleotide, we confirmed that the CXCL16 reporter regulation by miR-M23-2 could be inhibited in a sequence specific manner.
While the molecular basis of the escape remains to be unraveled (the chemokine CXCL16 was identified as a putative target of miR-M23-2, but is unlikely to be solely responsible for the phenotype), the study by Dlken and colleagues demonstrates the power of investigating miRNAs functions in the context of an authentic in vivo infection. It is unlikely that the phenotype would have been noticed by any other approach.