I certainly hope that you are looking into ERVs, Call_of_the_Wild, as knowledge of the issue will be necessary if you wish explain it within the scope of creationism. Perhaps you have already began looking at creationist websites which address the ERV issue. Be careful about what you read. Make sure that it is accurate, and of equal importance, up to date.
Here are some examples of arguments that I have found which creationist sites use to explain ERVs within the creationist model:
Some ERVs have functions within the human genome. As such, they must have been designed into the genome from the beginning and not inserted by viruses.
There are multiple problems with this argument. Firstly, there are many things about full-sequence ERVs that let us know they were inserted by retroviruses. Full-sequence ERVs have the same basic structure as known retroviral genomes. The structure of both is laid out as follows:
LTR-Gag-Pol-Env-LTR
The LTRs are "long terminal repeats" whereas Gag, Pol and Env are regions which code for the enzymes and proteins needed for the creation and transcription of viral particles. Since both known retroviruses and full-sequence ERVs have this same structure in this same order, we know that the ERVs came from retroviral insertions.
There's even more to it than that, however. An enzyme called "integrase" is used to insert the viral DNA into the host genome. One of the hallmarks of the action of this enzyme is "target site duplication", which causes an extra copy of DNA sections along the site where the retroviral genome has been inserted. As expected, full-sequence ERVs have these same target site duplications.
What's even more striking is the fact that ERVs can sometimes generate viral proteins and trigger retroviral antibody production by the immune system in humans. In Koalas, we even have an stronger example. Koala retrovirus (KoRV) is known to exist in both ERV form and as individual viral particles. Koalas can therefore transmit the virus either through typical disease route (from one adult to another) or by inheriting them from their parents (in ERV form). So we have an observed example of a retrovirus in the process of becoming an ERV.
As far as functionality in humans go, it should be noted that the LTRs are where ERVs express their function in humans. This is because LTRs can affect and control other genes in the human genome (as this is their function in retroviral genomes as well). The function seems to have simply been borrowed from the retroviruses once they became an integral part of the host genome. What's more important than this is the lack of function that the other components (gag-pol-env) have in the ERVs. Or if they do have function it is only from parts of them an not the package as a whole. If the ERVs were the product of design, you would then expect (1) that only the LTRs and other necessary bits would have been designed into the DNA and all of the other pieces left out as they have no function in humans (despite the fact that they do have critical functions in retroviruses) and (2) there would be no target site duplications.
There are only 7-14 ERVs common between humans and chimpanzees. Since retroviruses have a known degree of selectivity, we can explain a mere 7-14 ERVs out of 98,000 similarity by chance alone.
This argument is based on out-of-date information. It was true at one time that only 7 ERVs were known to be common between chimps and humans, but since 2005 the entirety of the chimpanzee genome has been sequenced. It was after doing this that scientists were able to discern that there was more than a 99.9% similarity between the ERV patterns between humans and chimpanzees. There is no possible way to account for this by chance alone. The selectivity of retroviruses is nowhere near sufficient.
This shows both (1) How we know that ERVs came from retroviral insertions and (2) how we know that they could not have gotten the same pattern by chance.
Take note of all of this before we begin our debate in chat, CotW.