[3] In 1958, Harry Rubin and Howard Temin developed an assay where chicken embryo fibroblasts could be altered morphologically by RSV infection.

These two findings gave rise to the notion that viral replication and malignant transformation are separate processes in RSV.

[3] RSV is a class VI enveloped virus with a positive sense RNA genome having a DNA intermediate.

[7] Very few acutely oncogenic or transforming retroviruses are capable of replication without a helper virus, making non-defective strains of RSV quite unique.

[9] It is an acquired gene, found to be present throughout the animal kingdom with high levels of conservation between species.

[4] The RNA genome of RSV contains an extremely long 3' UTR that ranges between 5–7 kb in length which would usually direct it toward nonsense mediated decay (NMD) within the eukaryotic host cell.

[12] The RSE element was first identified in the genome of the Rous Sarcoma Virus but appears to be widely conserved across the avian retrovirus family.

The RSE element is ~300 bp in length and located downstream of the gag natural translational termination codon.

The secondary structure of the RSE element has been determined by RNAse digestion and SHAPE chemistry analysis.

These cleaved products include the matrix (MA), capsid (CA), and nucleocapsid (NC), which are able to enter other pathways to infect new cells.