Here is a concise synopsis from Smilodon’s Retreat, here at SIN. I am fascinated with endogenous retroviruses (ERVs). It seems that they are simply not adequately explained on a creationism thesis. This usually entails trying to debunk them since they have no other answer!
Viruses are amazing things. I don’t think anyone would argue that they are actually living things. But they are extraordinarily complex systems and can have massive effects on organisms that as large to them as the a town is to us. Here’s a neat little animation that shows the scale of some viruses.
One particular class of virus is particularly interesting. We all should know about how most viruses work. They invade the cell, co-opt the organelles and make the cell do nothing but build new viruses. After some time, the cell dies, releasing all those new viruses into the host organism. The retroviruses are different.
I hesitate to use the word ‘insidious’, because they aren’t. They are just doing what they do. But to us, it seems insidious. Instead of just invading the cell and co-opting the organelles, a retrovirus actually inserts DNA into the genome of the cell.
A retrovirus is actually a RNA virus. The virus’s genetic material is stored as messenger RNA. The RNA is reverse transcribed into DNA in the host cell. Transcription is the process of forming an mRNA strand from DNA. Since the virus does the reverse, it’s a “retrovirus”. Retroviruses even have to bring a unique tool with them. The pol gene is responsible for making the viral reverse transcriptase, since cellular enzymes can’t perform that function.
So we have this unique mechanism in the retrovirus. But it gets more interesting. The viral DNA gets inserted into the host organism DNA. The cell then uses the viral DNA as a template for viral proteins. Instead of being co-opted, producing new viruses, and then dying, the cell lives it’s full life making new viral bodies along with everything else it’s supposed to do.
If the virus attacks a gamete, then that viral genome can appear in every cell in the offspring’s body and be passed on to future generations. It sounds like a great deal for the virus. However, the viruses are very sensitive. Viral genomes are often very tight, very compact, and very susceptible to mutation. Humans and other plants and animals (and other species as well) have multiple copies of each gene. So, if one of those alleles is broken by mutation, there is a spare. Viruses and bacteria don’t have this feature.
A mutation that damages the virus’s ability to perform any of the functions it must perform (invade a host cell, reverse transcribe the RNA, build the protein coat, etc) means that the virus is no longer effective. The entire genome is broken, the virus can no longer function, but the DNA is still there, in the host organism.
That is called an endogenous retrovirus (ERV).
How can this be evidence for evolution? Good question, I’m glad you asked.
Let’s say an organism gets one of these ERVs in its gametes and passes that gene onto it’s offspring. Except the offspring ends up with a mutation that breaks the viral gene (crossing over for example). Now, that organism has a gene that doesn’t affect anything, but it’s there.*
All of that organisms offspring will have a copy of that gene and, more telling, that gene will be in the same relative place. As time goes on and the species diverges, speciation events occur and mutations happen, a pattern will emerge. That pattern is the same as what is predicted for the idea of common descent. That is, organisms will share a common ancestor and those organisms that are more closely related will have a more recent common ancestor.
A 2000 study of primates shows this very well. All monkeys contain two particular ERVs. Another two ERVs are shared by all monkeys except new world monkeys. Three more are shared only by gibbons, orangutans. Another two are only shared between chimps, gorillas, and humans. And three more appear only in humans. This is but a tiny bit of the 30,000+ ERVs in our genome. A similar situation appears in felids.
If common descent were not correct, then we would not expect to see dozens of species with the exact same viral remnant in the exact same genomic position. For example, it would be highly unlike to find a cat with the same two ERVs shared by humans, chimps and gorillas.
If common descent were not correct, then we would not see a relationship between shared ERVs and the closeness of two species. The more closely related the organisms, the more ERVs they share.
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* There is significant evidence that ERV remnants do affect expression of other genes and that organisms can co-opt the former viral genes as well. But go with me here.
