Retroviruses are a class of virus that go through an RNA-to-DNA "reverse transcription" during their life cycle. Usually (in our cells and in many other types of viruses), DNA is used to make RNA, not the other way around. Everyone is familiar with at least one retrovirus, HIV. What most people are not familiar with is the fact that we carry around thousands of copies of retroviruses in our genomes. Since they appear to be "part" of our genomes (and also appear in chimpanzee genomes), they are called "endogenous retroviruses" or ERVs for short. Most of them have what appear to be "mutations" that prevent them from becoming infectious viruses (so you needn't worry about them). The standard explanation for ERVs is that they are left over from past infections or that they have copied themselves from leftovers of past infections. Over the years, they've become mutated and harmless.
In a creative twist, Liu and Soper suggest that it was actually the other way around: free retrovirus particles are actually escaped ERVs. It's an intriguing idea, and I like how they've sort of turned the standard model on its head to come up with a creationist explanation. Despite my enthusiasm for the idea, I really wish I could say that I liked the paper better. It's not that I disliked the paper, either. It's just that the authors didn't spend much time developing their hypothesis. Instead, they spend most of the paper on the "function" of ERVs, and their hypothesis unfortunately goes underdeveloped.
I have to give Liu and Soper credit though: they do a better job trying to establish the function of ERVs than most. Usually, creationists try to explain ERVs and similar sequences by giving a little catalogue of ERVs that have functions. Liu and Soper do indulge in that a little, for example, by citing the syncytin gene, which is an actual human gene that appears to be derived from an ERV. The frustrating part of all such catalogues is that they generally ignore three things: (1) the vast majority of ERVs for which no such function is known, (2) the transposability of ERVs (why intact ERVs can move around on their own), and (3) why they look like retroviruses in the first place.
As I said, Liu and Soper don't leave their paper at just that. They argue that since ERVs are transcriptionally regulated (that is, they become active at predictable times), they must have a function. That hypothesis is at the very least trying to put a global perspective on ERVs. I don't think it's quite as definitive as the authors do, but it's a very interesting observation.
In the end, though, I felt like the paper didn't need to argue for ERV function at all. Liu and Soper's hypothesis implies a number of things that could have been explored instead. For example, is there any evidence that specific retroviruses can be connected to specific ERVs? For their hypothesis to work, general resemblance is not enough; there must be particular sources of the various retroviruses. Have these sources been discovered or could they be (Liu and Soper did mention one endogenous virus that could have sourced the lentivirus-type retroviruses)? Another implication would be exploring the origin of other viruses. What about DNA viruses? Could they ultimately originate as escaped genomic elements from other critters? Do we know of any other kinds of endogenous viruses? Could this idea be expanded to a general theory of viral origin? These types of ideas get left behind in favor of explaining the function of ERVs.
Not that Liu and Soper's approach is wrong. Hypothesizing that the ERVs came first implies that they must have been put in the genome for a reason. From my perspective, that issue could have been addressed by simply pointing out that human ERVs are also present in chimpanzees, and since we have a separate origin (Genesis 2:7), those ERVs did not derive from a common ancestor - they were created as part of the overall similarity of chimp and human genomes. For the purpose of explaining the origin of retroviruses, I don't think we need to go into any more detail about the function of ERVs than appealing to their common design. I guess maybe the paper is mislabeled? It's more about ERV function with a suggestion about the origin of retroviruses in one section.
Ignoring the separate creation of humans and chimps also leads them to make an important error. Near the end of their paper, they made this claim:
In his book Genetic entropy and the mystery of the genome, Dr. John Sanford pointed out the degeneration of genomes and predicted the extinction of the human race (Sanford 2008). So the apparent degeneration of ERV elements in vertebrate genomes is real.Despite being a non sequitur, their conclusion does not follow from what we know about the origin of the human genome. Since the human and chimp genomes are very similar, the majority of ERVs are the same and have the same apparent "disabling mutations." Given the separate origins of humans and chimps (Genesis 2:7), we've either experienced thousands and thousands of mutations that are exactly the same as chimps or those "mutations" were created that way in the beginning. Since creation is the simpler hypothesis, that means the apparent degeneration of human and chimp ERVs is precisely that: apparent. Like ERVs themselves, the "disabling mutations" were also put there for a reason.
Now please don't think that I disliked this paper. I think that Liu and Soper's hypothesis is intriguing and deserving of further study. But the origin of retroviruses can be addressed separately from the function of ERVs. Liu and Soper seem to be more interested in ERV function, and their ideas about the transcriptional regulation are worth exploring. I just hope someone comes along to pick up the ball on retroviruses.
Liu and Soper. 2009. The Natural History of Retroviruses: Exogenization vs Endogenization. ARJ 2:97-106.