Before getting into the nitty gritty of endogenous retroviruses (ERVs), let’s start with a simple analogy to explain how the evidence works.
Let’s say you have two volunteers and two unabridged Oxford English Dictionaries. You give one dictionary to each person and tell them to go into separate rooms where they can’t see what the other is doing. You then ask them to randomly pick 100 words out of the dictionary and write them down on a sheet of paper. You bring them back into the same room and compare their list of words.
What would you expect? You would expect that few, if any, of the words should match. There are thousands and thousands of words in the OED and the chances of randomly matching nearly all 100 words from two random searches is highly improbable. As you would expect, none of the words match up. However, if you asked them to randomly find 1,000 words they may match a handful . . . maybe.
This is analogous to the way in which the ERV evidence works. In order for the retrovirus to replicate it has to insert its genome into the genome of the cell it has infected. Once in the host genome, the strong promoters in the viral genome cause the cell’s transcription and translation systems to make new viral particles from the genes in the viral genome. The process of inserting the viral genome into the host genome is quite random. If this happens in a gamete (i.e. egg or sperm), then it is possible for the viral insertion to be passed on to offspring. This is called an endogenous retrovirus, or ERV.
Due to the random nature of viral integration into the host genome we wouldn’t expect two independent insertion events to occur at the same position in two cells. The only reason we would expect to see large numbers of ERVs shared at the same position in two different genomes is if that insertion happened once in a common ancestor. The fact that you have about 200,000 ERVs in your genome that is shared by your siblings, extended family, and all other humans is testament to this process. Its not as if you and your cousin suffered 200,000 retroviral infections that just happened to produce the very same random insertions at the same spot in both of your genomes. The same logic applies to different species.
So how many ERVs do we share with other species? A lot of them. The human genome project found just over 200,000 ERVs in the human genome. When they sequenced the chimp genome they found that 82 of those human ERVs were not found at the same spot in the chimp genome. More than 99.9% of human ERVs were found at the same spot in the chimp genome. nearly all 200,000 of them. This couldn’t happen by random independent events. This can only happen by common ancestry.
References.
Human genome paper, table 11:
http://www.nature.com/nature/journal/v409/n6822/fig_tab/409860a0_T11.html
Chimp genome paper, table 2:
http://www.nature.com/nature/journal/v437/n7055/fig_tab/nature04072_T2.html
There is also evidence in the ERV sequences themselves that provide more independent lines of evidence for common ancestry, such as LTR divergence. These are bit more complicated and probably not conducive to the type of conversation you are having with your pastor. There are also many common creationist arguments which I could cover. Such as:
How do you know that ERVs are from retroviruses?
Is retroviral insertion random?
How do you know that God didn’t create these genomes with the ERVs already in them (i.e. the Omphalos argument)?
If any of these interest you I would be happy to discuss them, or answer any other questions that you may have.