Animal genomes are known to contain captured retroviruses, typically referred to as endogenous retroviruses (ERVs). Many of these elements are still transcribed and are known to be involved in both beneficial functions in animal biology, such as placenta formation, and not-so beneficial functions such as certain auto-immune diseases as well as cancer. Interestingly, in some cases, such as in ERVs from sheep, they actually protect their hosts from exogenous (incoming) retroviruses.
However, it is not often mentioned that Bornaviruses, non-segmented RNA viruses that replicate in the nuclei of their hosts, have also been shown to be endogenous viruses in several mammalian host genomes including humans, non-human primates, rodents and elephants. This is especially interesting given that these viruses do not integrate into their host genomes as a part of their normal replication cycle. This implies that at some point in mammalian evolution, a bornavirus relative relied on a host-derived mechanism, probably retrotransposons, for its capture and subsequent endogenization. The portion of the endogenous bornavirus (EnBVs) genome predominantly encodes the viral nucleocapsid. Previous studies have found that the bornavirus nucleocapsid protects cells from subsequent bornavirus infections.
In this study, the authors cloned sequences from an endogenous bornavirus of squirrels into a cell line, and monitored both its solitary activity and how it interacts with an exogenous bornavirus. They found that this transcript encoded a protein that co-localized within the viral replication factory of the exogenous bornavirus in the nucleus. Not only did this protein result in a reduced level of replication of the introduced bornavirus, but cells stably expressing the EnBV protein were completely resistant to exogenous bornaviruses. They then went on to show that the protein "appeared to affect BDV polymerase activity by being incorporated into the viral ribonucleoprotein". Interestingly, the human version of the EnBV did not have this same effect.