ABSTRACT
The murine polyoma virus model system has provided a convenient system in which to study the mechanism of action of nuclear antisense RNA. At late times in the polyoma virus life cycle, nuclear antisense RNA is used to downregulate the expression of viral “early” genes. Further, nuclear antisense RNAs appeared to be more effective inhibitors of the target gene expression than comparable polyadenylated antisense molecules, which were transported to the cytoplasm. More recent work has demonstrated that nuclear antisense RNA can also act in co-transfection studies to efficiently reduce mRNA levels from an HIV-1 subgenomic expression construct. Antisense expression should be driven from a promoter appropriate for the level of the expression desired and the cells to be targeted. There are of course a very large number of available promoters that can be chosen, including both constitutive and inducible ones.
