Since EGS C2, with the point mutations at the T-loop (Figure 1(d)), exhibited little targeting activity but bound to the targeted CCR5 mRNA sequence as well as EGS C1, these observations suggest that the significant inhibition of HIV infection in cells that expressed C1 was due to the RNase P-mediated cleavage of the target CCR5 mRNA directed by the EGS. Here, CCR5 is linked to HIV infectious disease.