KoRV might be a good example to look at. This is a retrovirus that is currently invading the genomes of modern Koala populations:
I would think that ERV’s are going to evolve much slower in the host than the sequences in the viral population, so it may be difficult to differentiate between mutations that occur in each population. Larger scale changes might be easier to detect, such as recombination between ERV’s.
It is my understanding that there are three main models of virus origins, but in fact all three scenarios may be correct to some extend.
In one model, viruses evolved from selfish genetic elements and learned to move between cells. In another model, selfish genetic elements evolved by reductive evolution from viruses. And in the third model, viruses came before even cellular life, and they later co-evolved with cellular life.
It is of course possible that some mix of these different scenarios are possible; That some viruses evolved from selfish genetic elements, that some selfish genetic elements evolved from ancient retroviral infections, and even that this has occurred while both viruses and cellular life co-evolved since the origin of life.
I’m not well read on this topic at all, so for concrete examples of which viruses, and which retroviruses evolved from each other your googling will be as good as mine.
For the sake of argument, let’s say there is this crazy event that recombines all of these different host genes and what you get is a retroviral genome (i.e. a de novo retrovirus). Then what? How does it infect other organisms and cells?
From where I sit, it would have to go through the usual retroviral cycle. It would attach to a cell, expel its guts into the cell, insert its genome into the host genome, express the viral genes using the host transcriptional systems, have the different parts interact and form a viral particle, have that viral particle released from the cell, and then repeat. This would produce new ERV’s in the host genome.
We could also look at modern retroviruses. There are no widespread HIV ERV’s in the human population that I am aware of, so the source of those infections must be exogenous retrovirus.
If we are looking at hundreds of thousands of ERV’s in a vertebrate genome it seems much more likely that they are due to viral infections than a de novo ERV. In between, I can see the virus to ERV to virus route. Viruses produce ERV’s which recombine to form new viruses. ERV’s are known for recombining with themselves due to the repetitive DNA at each end of the genome, producing solo LTR’s, so it wouldn’t be surprising if this could happen between ERV’s.
This is the kind of thread which brings me to Peaceful Science each day. I have a very basic understanding of ERVs, retroviruses, and the lysogenic cycle but this discussion has already taken me into territory I had never considered. Joshua’s simple but fascinating question (“Are there any examples of it being co-opted or evolving into a virus again?”) drew helpful responses from our scientists. Thank you!
Very educational. I feel privileged to benefit from the expertise of the many scientists here on PS.
HERVs, retroviral sequences integrated into the genome during evolution, are now known to represent 8% of the human genome.
These were recently shown to comprise copies that retain potential to express retroviral proteins or particles, and can be abnormally expressed in autoimmune, neurodegenerative, chronic inflammatory diseases, and cancer.
Environmental factors such as specific viral infections were shown to potently activate HERVs under tissue-specific and temporal conditions.
Of several diseases in which abnormal activation and expression of HERV proteins have been reported, studies over recent decades have led to a proof of concept that HERVs play a key role in the pathogenesis of MS and ALS.
HERV-W and HERV-K Env proteins induce pathogenic effects in vitro and in vivo that are relevant to the pathognomonic features of these diseases.
These endogenous retroviruses are potential novel therapeutic targets that are now being addressed with innovative therapeutic strategies in clinical trials.
The causes of multiple sclerosis and amyotrophic lateral sclerosis have long remained elusive. A new category of pathogenic components, normally dormant within human genomes, has been identified: human endogenous retroviruses (HERVs). These represent ∼8% of the human genome, and environmental factors have reproducibly been shown to trigger their expression. The resulting production of envelope (Env) proteins from HERV-W and HERV-K appears to engage pathophysiological pathways leading to the pathognomonic features of MS and ALS, respectively. Pathogenic HERV elements may thus provide a missing link in understanding these complex diseases. Moreover, their neutralization may represent a promising strategy to establish novel and more powerful therapeutic approaches.
say that all creatures were designed for the sake of the argument. and all of them had ervs in the first place. lets consider them to be genes, like any other genes in the genome. where do you see any problem under that scenario?
It doesn’t explain the multiple examples of phylogenetic signals, such as LTR divergence. There are at least 3 levels of evidence that would need to be explained by your scenario, and I don’t see how it could be done:
As with almost all of these discussions, it boils down to the phylogenetic evidence.