I'm not sure that happens with human genomes, either. I tend to think it's unlikely, simply because it seems improbable that human genomes experience any meaningful selection pressure for information density.
Virus particles are typically very small, and viral genomes thus need to cram whatever they require into as little space as possible - being more information-dense means being able to fit more genes and thus more functionality, which I should think would be a pretty significant adaptive advantage.
Human cell nuclei, by contrast, are quite roomy - by a virus's standards, practically palatial, given that the largest known viral genome is about 0.03x the size of a human one. As it is, all our chromosomes fit into the nucleus with a good deal of space left over, and still could do even if considerably larger than they actually are right now. So, while a mechanism like you describe certainly could evolve, it'd be under no special pressure to do so.
That seems to be a different process, occurring at a different stage of expression - the link describes different ways eukaryotic mRNA can be spliced prior to translation; grandparent comment refers to a detail of how the translation process itself works with viral mRNA.
Specifically, that reference appears to be to one of apparently several mechanisms of non-canonical translation in viral RNA [1]:
> The focus is on the different translational strategies that RNA viruses employ for accessing multiple ORFs in mRNAs.
An "ORF", or "open reading frame", is a translatable sequence of bases, usually understood to begin immediately after a common "header" sequence at the start of an RNA strand. But viral genomes appear to have not even just one trick, but a whole bag of them, for getting host ribosomes to translate the same genome in multiple ways, as grandparent commenter describes. Which is really neat!
Also, it looks like I should've done some literature review before my own prior comment. Per [2], ribosome profiling - a technique which may be newer than my own experience in the field [3], and of which I was in any case unaware - has been used to show that eukaryotic RNAs likewise can and perhaps frequently do encode multiple ORFs which are routinely translated. Which is also really neat!
[3] What appears to be the seminal paper for modern ribosome profiling [4] was published in early 2014, more or less at the same time I left the organization where I might have heard about it.
Virus particles are typically very small, and viral genomes thus need to cram whatever they require into as little space as possible - being more information-dense means being able to fit more genes and thus more functionality, which I should think would be a pretty significant adaptive advantage.
Human cell nuclei, by contrast, are quite roomy - by a virus's standards, practically palatial, given that the largest known viral genome is about 0.03x the size of a human one. As it is, all our chromosomes fit into the nucleus with a good deal of space left over, and still could do even if considerably larger than they actually are right now. So, while a mechanism like you describe certainly could evolve, it'd be under no special pressure to do so.