Transposons (TEs) cause fusion proteins and aneuploidy

New studies revealed that the genome is dynamic, driven  by transposons and controlled by epigenesis. These  studies unveil also  a complex  and vibrating genome, in which mutations are formed and deleted, amidst  a continuous transposon turnover. Transposable elements constitute   50%  the human genome.  They are highly  mutagenic,  targeting protein-coding genes for insertion,  causing chromosome breakage  and genome rearrangement.

Epigenesis controls TEs by several mechanisms:
- A range of chromatin modifications suppress TE  transcription.
- Post-transcriptional silencing of TEs by RNAi.
- Proteins that modify chromatin structure are also involved in TE silencing.

The response of TEs to stress can occur through one of  two mechanisms 
First, the stress could directly activate TEs and their mutagenic activity.
Second, stress might inhibit gene-silencing mechanisms in the genome, indirectly resulting in the reactivation of TEs.

There is an important biological law which ought to be considered when explaining biological phenomena. A living entity under stress (perturbation) will restructure itself so as to maximize its survival.

Virus is the stress agent that activates TEs to reshuffle  the genome in order to maximize survival.

Stress activated TEs  reshuffle the genome, so as to maximize the survival of the entity carrying it. Reshuffling generates  fusion genes (chimeric transcripts), which enable the entity to continue living.